Ferroptosis-centered Disease Response Information
General Information of the Disease (ID: DIS00042)
Name |
Cervical cancer
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ICD |
ICD-11: 2C77
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Full List of Target(s) of This Ferroptosis-centered Disease
Heat shock protein beta-1 (HSPB1)
In total 2 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target | [1] | ||||
Target for Ferroptosis | Marker/Suppressor | ||||
Responsed Disease | Endocervical adenocarcinoma [ICD-11: 2C77] | ||||
Responsed Drug | Erastin | Investigative | |||
Responsed Regulator | Heat shock factor protein 1 (HSF1) | Suppressor | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model | HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 | |
U2OS cells | Osteosarcoma | Homo sapiens | CVCL_0042 | ||
LNCaP cells | Prostate carcinoma | Homo sapiens | CVCL_0395 | ||
In Vivo Model |
Indicated HeLa cells were subcutaneously injected into the dorsal flanks right of the midline in SCID mice (weight ~20 g). At day seven, mice were injected with erastin (20 mg/kg/ i.v., twice daily every other day) with or without KRIBB3 (50 mg/kg/ i.p., once daily every other day) for two weeks. Erastin was dissolved in vehicle (2% DMSO and 98% phosphate buffered saline) and prepared by Ultrasonic Cleaner (Fisher Scientific). A final volume of 300 ul erastin was applied through the tail vein. The Rodent Tail Vein Catheter (Braintree Scientific, MTV#1) were used to perform injection.
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Response regulation | Erastin, a specific ferroptosis-inducing compound, stimulates heat shock factor 1 ( HSF1)-dependent HSPB1 expression in endocervical adenocarcinoma cells. Knockdown of HSF1 and HSPB1 enhances erastin-induced ferroptosis, whereas heat shock pretreatment and overexpression of HSPB1 inhibits erastin-induced ferroptosis. | ||||
Experiment 2 Reporting the Ferroptosis-centered Disease Response by This Target | [1] | ||||
Target for Ferroptosis | Marker/Suppressor | ||||
Responsed Disease | Endocervical adenocarcinoma [ICD-11: 2C77] | ||||
Responsed Drug | Erastin | Investigative | |||
Responsed Regulator | Heat shock factor protein 1 (HSF1) | Suppressor | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model | HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 | |
U2OS cells | Osteosarcoma | Homo sapiens | CVCL_0042 | ||
LNCaP cells | Prostate carcinoma | Homo sapiens | CVCL_0395 | ||
In Vivo Model |
Indicated HeLa cells were subcutaneously injected into the dorsal flanks right of the midline in SCID mice (weight ~20 g). At day seven, mice were injected with erastin (20 mg/kg/ i.v., twice daily every other day) with or without KRIBB3 (50 mg/kg/ i.p., once daily every other day) for two weeks. Erastin was dissolved in vehicle (2% DMSO and 98% phosphate buffered saline) and prepared by Ultrasonic Cleaner (Fisher Scientific). A final volume of 300 ul erastin was applied through the tail vein. The Rodent Tail Vein Catheter (Braintree Scientific, MTV#1) were used to perform injection.
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Response regulation | Erastin, a specific ferroptosis-inducing compound, stimulates heat shock factor 1 (HSF1)-dependent HSPB1 expression in endocervical adenocarcinoma cells. Knockdown of HSF1 and HSPB1 enhances erastin-induced ferroptosis, whereas heat shock pretreatment and overexpression of HSPB1 inhibits erastin-induced ferroptosis. | ||||
Cytochrome b-245 heavy chain (CYBB)
In total 5 item(s) under this target | ||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target | [2] | |||
Target for Ferroptosis | Driver | |||
Responsed Disease | Endocervical adenocarcinoma [ICD-11: 2C77] | |||
Responsed Drug | Hydrogen Peroxide | Investigative | ||
Responsed Regulator | Aquaporin-3 (AQP3) | Driver | ||
Pathway Response | Fatty acid metabolism | hsa01212 | ||
Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | |||
In Vitro Model | HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 |
SAS cells | Tongue squamous cell carcinoma | Homo sapiens | CVCL_1675 | |
Response regulation | Mitochondrial transfer upregulated the mitochondrial quality control protein prohibitin 2 (PHB2), which contributes to reduced AQPs( AQP3, AQP5,AQP8) expression. H2O2 treatment enhances AQPs expression, Fe2+ level, and lipid peroxidation, and decrease mitochondrial function by downregulating PHB2 in endocervical adenocarcinoma, and thus, is a promising modality for effective cancer treatment. Moreover, NOX2 expression is upregulated in 0 cells, and that NOX2 binds to AQP3, 5, and 8 in both HeLa and SAS cells. | |||
Experiment 2 Reporting the Ferroptosis-centered Disease Response by This Target | [2] | |||
Target for Ferroptosis | Driver | |||
Responsed Disease | Endocervical adenocarcinoma [ICD-11: 2C77] | |||
Responsed Drug | Hydrogen Peroxide | Investigative | ||
Responsed Regulator | Aquaporin-5 (AQP5) | Driver | ||
Pathway Response | Fatty acid metabolism | hsa01212 | ||
Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | |||
In Vitro Model | HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 |
SAS cells | Tongue squamous cell carcinoma | Homo sapiens | CVCL_1675 | |
Response regulation | Mitochondrial transfer upregulated the mitochondrial quality control protein prohibitin 2 (PHB2), which contributes to reduced AQPs(AQP3, AQP5,AQP8) expression. H2O2 treatment enhances AQPs expression, Fe2+ level, and lipid peroxidation, and decrease mitochondrial function by downregulating PHB2 in endocervical adenocarcinoma, and thus, is a promising modality for effective cancer treatment. Moreover, NOX2 expression is upregulated in 0 cells, and that NOX2 binds to AQP3, 5, and 8 in both HeLa and SAS cells. | |||
Experiment 3 Reporting the Ferroptosis-centered Disease Response by This Target | [2] | |||
Target for Ferroptosis | Driver | |||
Responsed Disease | Endocervical adenocarcinoma [ICD-11: 2C77] | |||
Responsed Drug | Hydrogen Peroxide | Investigative | ||
Responsed Regulator | Aquaporin-8 (AQP8) | Driver | ||
Pathway Response | Fatty acid metabolism | hsa01212 | ||
Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | |||
In Vitro Model | HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 |
SAS cells | Tongue squamous cell carcinoma | Homo sapiens | CVCL_1675 | |
Response regulation | Mitochondrial transfer upregulated the mitochondrial quality control protein prohibitin 2 (PHB2), which contributes to reduced AQPs(AQP3, AQP5, AQP8) expression. H2O2 treatment enhances AQPs expression, Fe2+ level, and lipid peroxidation, and decrease mitochondrial function by downregulating PHB2 in endocervical adenocarcinoma, and thus, is a promising modality for effective cancer treatment. Moreover, NOX2 expression is upregulated in 0 cells, and that NOX2 binds to AQP3, 5, and 8 in both HeLa and SAS cells. | |||
Experiment 4 Reporting the Ferroptosis-centered Disease Response by This Target | [2] | |||
Target for Ferroptosis | Driver | |||
Responsed Disease | Endocervical adenocarcinoma [ICD-11: 2C77] | |||
Responsed Drug | Hydrogen Peroxide | Investigative | ||
Responsed Regulator | Aquaporin-8 (AQP8) | Driver | ||
Pathway Response | Fatty acid metabolism | hsa01212 | ||
Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | |||
In Vitro Model | HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 |
SAS cells | Tongue squamous cell carcinoma | Homo sapiens | CVCL_1675 | |
Response regulation | Mitochondrial transfer upregulated the mitochondrial quality control protein prohibitin 2 (PHB2), which contributes to reduced AQPs(AQP3, AQP5,AQP8) expression. H2O2 treatment enhances AQPs expression, Fe2+ level, and lipid peroxidation, and decrease mitochondrial function by downregulating PHB2 in endocervical adenocarcinoma, and thus, is a promising modality for effective cancer treatment. Moreover, NOX2 expression is upregulated in 0 cells, and that NOX2 binds to AQP3, 5, and 8 in both HeLa and SAS cells. | |||
Experiment 5 Reporting the Ferroptosis-centered Disease Response by This Target | [2] | |||
Target for Ferroptosis | Driver | |||
Responsed Disease | Endocervical adenocarcinoma [ICD-11: 2C77] | |||
Responsed Drug | Hydrogen Peroxide | Investigative | ||
Responsed Regulator | Aquaporin-3 (AQP3) | Driver | ||
Pathway Response | Fatty acid metabolism | hsa01212 | ||
Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | |||
In Vitro Model | HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 |
SAS cells | Tongue squamous cell carcinoma | Homo sapiens | CVCL_1675 | |
Response regulation | Mitochondrial transfer upregulated the mitochondrial quality control protein prohibitin 2 (PHB2), which contributes to reduced AQPs(AQP3, AQP5,AQP8) expression. H2O2 treatment enhances AQPs expression, Fe2+ level, and lipid peroxidation, and decrease mitochondrial function by downregulating PHB2 in endocervical adenocarcinoma, and thus, is a promising modality for effective cancer treatment. Moreover, NOX2 expression is upregulated in 0 cells, and that NOX2 binds to AQP3, 5, and 8 in both HeLa and SAS cells. | |||
Polyunsaturated fatty acid lipoxygenase ALOX12 (ALOX12)
In total 1 item(s) under this target | ||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target | [3] | |||
Target for Ferroptosis | Driver | |||
Responsed Disease | Endocervical adenocarcinoma [ICD-11: 2C77] | |||
Responsed Regulator | hsa-miR-7-5p (miRNA) | Suppressor | ||
Pathway Response | Fatty acid metabolism | hsa01212 | ||
Cell Process | Cell ferroptosis | |||
In Vitro Model | HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 |
SAS cells | Tongue squamous cell carcinoma | Homo sapiens | CVCL_1675 | |
Response regulation | Knockdown of miR-7-5p increased reactive oxygen species (ROS), mitochondrial membrane potential, and intracellular Fe2+amount. Furthermore, miR-7-5p knockdown results in the down-regulation of the iron storage gene expression such as ferritin, up-regulation of the ferroptosis marker ALOX12 gene expression, and increases of Liperfluo amount in Endocervical adenocarcinoma. | |||
Phospholipid hydroperoxide glutathione peroxidase (GPX4)
In total 3 item(s) under this target | ||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target | [4] | |||
Target for Ferroptosis | Suppressor | |||
Responsed Disease | Cervical cancer [ICD-11: 2C77.Z] | |||
Responsed Drug | Dihydroartemisinin | Investigative | ||
Pathway Response | Fatty acid metabolism | hsa01212 | ||
Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | |||
In Vitro Model | HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 |
SiHa cells | Cervical squamous cell carcinoma | Homo sapiens | CVCL_0032 | |
Response regulation | Dihydroartemisinin (DHA) treatment initiated ferroptosis, as evidenced by the accumulation of reactive oxygen species (ROS), malondialdehyde (MDA) and liquid peroxidation (LPO) levels and simultaneously depletion of glutathione peroxidase 4 (GPX4) and glutathione (GSH). Moreover, nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy was also induced by DHA leading to subsequent increases of intracellular labile iron pool (LIP), exacerbated the Fenton reaction resulting in excessive ROS production, and enhanced cervical cancer ferroptosis. | |||
Experiment 2 Reporting the Ferroptosis-centered Disease Response by This Target | [5] | |||
Target for Ferroptosis | Suppressor | |||
Responsed Disease | Cervical cancer [ICD-11: 2C77.Z] | |||
Responsed Regulator | hsa-miR-193a-5p (miRNA) | Driver | ||
Pathway Response | Ferroptosis | hsa04216 | ||
Fatty acid metabolism | hsa01212 | |||
Cell Process | Cell ferroptosis | |||
In Vitro Model | SiHa cells | Cervical squamous cell carcinoma | Homo sapiens | CVCL_0032 |
HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 | |
Response regulation | miR-193a-5p was able to target GPX4 and circACAP2 promoted GPX4 expression by sponging miR-193a-5p in cervical cancer cells.Therefore, we concluded that circular RNA circACAP2 repressed ferroptosis of cervical cancer during malignant progression by miR-193a-5p/GPX4. | |||
Experiment 3 Reporting the Ferroptosis-centered Disease Response by This Target | [5] | |||
Target for Ferroptosis | Suppressor | |||
Responsed Disease | Cervical cancer [ICD-11: 2C77.Z] | |||
Responsed Regulator | CircACAP2 (circRNA) | Suppressor | ||
Pathway Response | Ferroptosis | hsa04216 | ||
Fatty acid metabolism | hsa01212 | |||
Cell Process | Cell ferroptosis | |||
In Vitro Model | SiHa cells | Cervical squamous cell carcinoma | Homo sapiens | CVCL_0032 |
HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 | |
Response regulation | miR-193a-5p was able to target GPX4 and circACAP2 promoted GPX4 expression by sponging miR-193a-5p in cervical cancer cells.Therefore, we concluded that circular RNA circACAP2 repressed ferroptosis of cervical cancer during malignant progression by miR-193a-5p/GPX4. | |||
Nuclear receptor coactivator 4 (NCOA4)
In total 1 item(s) under this target | ||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target | [4] | |||
Target for Ferroptosis | Driver | |||
Responsed Disease | Cervical cancer [ICD-11: 2C77.Z] | |||
Responsed Drug | Dihydroartemisinin | Investigative | ||
Pathway Response | Fatty acid metabolism | hsa01212 | ||
Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | |||
In Vitro Model | HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 |
SiHa cells | Cervical squamous cell carcinoma | Homo sapiens | CVCL_0032 | |
Response regulation | Dihydroartemisinin (DHA) treatment initiated ferroptosis, as evidenced by the accumulation of reactive oxygen species (ROS), malondialdehyde (MDA) and liquid peroxidation (LPO) levels and simultaneously depletion of glutathione peroxidase 4 (GPX4) and glutathione (GSH). Moreover, nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy was also induced by DHA leading to subsequent increases of intracellular labile iron pool (LIP), exacerbated the Fenton reaction resulting in excessive ROS production, and enhanced cervical cancer ferroptosis. | |||
Long-chain-fatty-acid--CoA ligase 4 (ACSL4)
In total 3 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target | [6] | ||||
Target for Ferroptosis | Driver | ||||
Responsed Disease | Cervical cancer [ICD-11: 2C77.Z] | ||||
Responsed Drug | Oleanolic acid | Investigative | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model | HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 | |
In Vivo Model |
Male BALB/c Nude mice (20 ± 2g, 5 weeks old) were supplied by Hangzhou Ziyuan Experimental Animal Technology Co. LTD (SYXK-20180049) for this study. The nude mice were kept under specefic pathogen free (SPF) conditions for one week, and 5x107 Hela cells were injected under the left axillary skin after acclimatization. The tumors of Hela cell-inoculated mice were measured every 3 days after modeling, and tumor>=0.5 cm in diameter were considered successful. The tumor-bearing mice were randomly divided into control group (n = 6), 40 mg/kg OA group (n = 6) and 80 mg/kg OA group (n = 6). 40 mg/kg OA group and 80 mg/kg OA group both received subcutaneous injection modeling and control mice received saline intraperitoneal injections. The 40 mg/kg OA group and 80 mg/kg OA group received daily intraperitoneal injections of 40 mg/kg OA and 80 mg/kg OA for 15 days.
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Response regulation | Oleanolic acid (OA) significantly reduced the viability and proliferative capacity of Hela cells. OA activated ferroptosis in Hela cells by promoting ACSL4 expression, thereby reducing the survival rate of Hela cells. Therefore, promotion of ACSL4-dependent ferroptosis by OA may be a potential approach for the treatment of cervical cancer. | ||||
Experiment 2 Reporting the Ferroptosis-centered Disease Response by This Target | [7] | ||||
Target for Ferroptosis | Driver | ||||
Responsed Disease | Cervical cancer [ICD-11: 2C77.Z] | ||||
Responsed Regulator | CircLMO1 (circRNA) | Driver | |||
Pathway Response | Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
Cell invasion | |||||
In Vitro Model | SiHa cells | Cervical squamous cell carcinoma | Homo sapiens | CVCL_0032 | |
HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 | ||
Ca Ski cells | Cervical squamous cell carcinoma | Homo sapiens | CVCL_1100 | ||
C33A cells | Cervical squamous cell carcinoma | Homo sapiens | CVCL_1094 | ||
In Vivo Model |
Male BALB/c nude mice (6 weeks old) were purchased from Beijing Vital River Laboratory Animal Technology Co., Ltd. (Beijing, China). The mice were kept in a constant temperature (25) and pathogen-free room with free access to food and water ad libitum. The animal experiments were approved by the Ethics Committee for Animal Experimentation of The Second Affiliated Hospital and Yuying Childrens Hospital. Mice were euthanised with isoflurane inhalation. CaSki cells overexpressing circLMO1 (7 x 106 cells/100 uL PBS) were injected subcutaneously into the flank of mice. Tumor growth was measured with a caliper 3 times a week and tumor-bearing mice were euthanised at 5 weeks after inoculation.
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Response regulation | CircLMO1 acted as a competing endogenous RNA (ceRNA) by sponging miR-4192 to repress target gene ACSL4. CircLMO1 promoted cervical cancer cell ferroptosis through up-regulating ACSL4 expression. Overexpression of miR-4291 or knockdown of ACSL4 reversed the effect of circLMO1 on facilitating ferroptosis and repressing cervical cancer cell proliferation and invasion. | ||||
Experiment 3 Reporting the Ferroptosis-centered Disease Response by This Target | [7] | ||||
Target for Ferroptosis | Driver | ||||
Responsed Disease | Cervical cancer [ICD-11: 2C77.Z] | ||||
Responsed Regulator | hsa-miR-4291 (miRNA) | Suppressor | |||
Pathway Response | Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
Cell invasion | |||||
In Vitro Model | SiHa cells | Cervical squamous cell carcinoma | Homo sapiens | CVCL_0032 | |
HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 | ||
Ca Ski cells | Cervical squamous cell carcinoma | Homo sapiens | CVCL_1100 | ||
C33A cells | Cervical squamous cell carcinoma | Homo sapiens | CVCL_1094 | ||
In Vivo Model |
Male BALB/c nude mice (6 weeks old) were purchased from Beijing Vital River Laboratory Animal Technology Co., Ltd. (Beijing, China). The mice were kept in a constant temperature (25) and pathogen-free room with free access to food and water ad libitum. The animal experiments were approved by the Ethics Committee for Animal Experimentation of The Second Affiliated Hospital and Yuying Childrens Hospital. Mice were euthanised with isoflurane inhalation. CaSki cells overexpressing circLMO1 (7 x 106 cells/100 uL PBS) were injected subcutaneously into the flank of mice. Tumor growth was measured with a caliper 3 times a week and tumor-bearing mice were euthanised at 5 weeks after inoculation.
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Response regulation | CircLMO1 acted as a competing endogenous RNA (ceRNA) by sponging miR-4192 to repress target gene ACSL4. CircLMO1 promoted cervical cancer cell ferroptosis through up-regulating ACSL4 expression. Overexpression of miR-4291 or knockdown of ACSL4 reversed the effect of circLMO1 on facilitating ferroptosis and repressing cervical cancer cell proliferation and invasion. | ||||
Cystine/glutamate transporter (SLC7A11)
In total 4 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target | [8] | ||||
Target for Ferroptosis | Suppressor | ||||
Responsed Disease | Cervical cancer [ICD-11: 2C77.Z] | ||||
Responsed Regulator | CircEPSTI1 (circRNA) | Suppressor | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model | Ca Ski cells | Cervical squamous cell carcinoma | Homo sapiens | CVCL_1100 | |
HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 | ||
hCECs (Human cervical epithelial cells) | |||||
In Vivo Model |
The 4-week-old female BALB/c nude mice were used for constructing xenograft model. HeLa cells (1 x 107 cells/mL) were injected into the dorsal flanksusing using 1-mL syringes. Then tumor size was measured and mice received intertumoral injection of si-crEPSTI1-1 (40 uL siRNA1 for cicrEPSTI1) and negative control (40 uL negative control) every four days, respectively (5 mice/group). After 28 days, the mice were sacrificed and xenografts were measured.
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Response regulation | CircEPSTI1 sponges miR-375, miR-409-3p and miR-515-5p to upregulate SLC7A11 expression. CircEPSTI1-miR-375/409-3P/515-5p-SLC7A11 axis affected the proliferation of cervical cancer via the competing endogenous RNAs (ceRNA) mechanism and was relative to ferroptosis. | ||||
Experiment 2 Reporting the Ferroptosis-centered Disease Response by This Target | [8] | ||||
Target for Ferroptosis | Suppressor | ||||
Responsed Disease | Cervical cancer [ICD-11: 2C77.Z] | ||||
Responsed Regulator | hsa-miR-375-3p (miRNA) | Driver | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model | Ca Ski cells | Cervical squamous cell carcinoma | Homo sapiens | CVCL_1100 | |
HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 | ||
hCECs (Human cervical epithelial cells) | |||||
In Vivo Model |
The 4-week-old female BALB/c nude mice were used for constructing xenograft model. HeLa cells (1 x 107 cells/mL) were injected into the dorsal flanksusing using 1-mL syringes. Then tumor size was measured and mice received intertumoral injection of si-crEPSTI1-1 (40 uL siRNA1 for cicrEPSTI1) and negative control (40 uL negative control) every four days, respectively (5 mice/group). After 28 days, the mice were sacrificed and xenografts were measured.
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Response regulation | CircEPSTI1 sponges miR-375, miR-409-3p and miR-515-5p to upregulate SLC7A11 expression. CircEPSTI1- miR-375/409-3P/515-5p-SLC7A11 axis affected the proliferation of cervical cancer via the competing endogenous RNAs (ceRNA) mechanism and was relative to ferroptosis. | ||||
Experiment 3 Reporting the Ferroptosis-centered Disease Response by This Target | [8] | ||||
Target for Ferroptosis | Suppressor | ||||
Responsed Disease | Cervical cancer [ICD-11: 2C77.Z] | ||||
Responsed Regulator | hsa-miR-409-3p (miRNA) | Driver | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model | Ca Ski cells | Cervical squamous cell carcinoma | Homo sapiens | CVCL_1100 | |
HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 | ||
hCECs (Human cervical epithelial cells) | |||||
In Vivo Model |
The 4-week-old female BALB/c nude mice were used for constructing xenograft model. HeLa cells (1 x 107 cells/mL) were injected into the dorsal flanksusing using 1-mL syringes. Then tumor size was measured and mice received intertumoral injection of si-crEPSTI1-1 (40 uL siRNA1 for cicrEPSTI1) and negative control (40 uL negative control) every four days, respectively (5 mice/group). After 28 days, the mice were sacrificed and xenografts were measured.
Click to Show/Hide
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Response regulation | CircEPSTI1 sponges miR-375, miR-409-3p and miR-515-5p to upregulate SLC7A11 expression. CircEPSTI1-miR-375/ 409-3P/515-5p-SLC7A11 axis affected the proliferation of cervical cancer via the competing endogenous RNAs (ceRNA) mechanism and was relative to ferroptosis. | ||||
Experiment 4 Reporting the Ferroptosis-centered Disease Response by This Target | [8] | ||||
Target for Ferroptosis | Suppressor | ||||
Responsed Disease | Cervical cancer [ICD-11: 2C77.Z] | ||||
Responsed Regulator | hsa-miR-515-5p (miRNA) | Driver | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model | Ca Ski cells | Cervical squamous cell carcinoma | Homo sapiens | CVCL_1100 | |
HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 | ||
hCECs (Human cervical epithelial cells) | |||||
In Vivo Model |
The 4-week-old female BALB/c nude mice were used for constructing xenograft model. HeLa cells (1 x 107 cells/mL) were injected into the dorsal flanksusing using 1-mL syringes. Then tumor size was measured and mice received intertumoral injection of si-crEPSTI1-1 (40 uL siRNA1 for cicrEPSTI1) and negative control (40 uL negative control) every four days, respectively (5 mice/group). After 28 days, the mice were sacrificed and xenografts were measured.
Click to Show/Hide
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Response regulation | CircEPSTI1 sponges miR-375, miR-409-3p and miR-515-5p to upregulate SLC7A11 expression. CircEPSTI1-miR-375/409-3P/ 515-5p-SLC7A11 axis affected the proliferation of cervical cancer via the competing endogenous RNAs (ceRNA) mechanism and was relative to ferroptosis. | ||||
Unspecific Target
In total 3 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target | [9] | ||||
Responsed Disease | Endocervical adenocarcinoma [ICD-11: 2C77] | ||||
Responsed Drug | Gallic acid | Investigative | |||
Pathway Response | Ferroptosis | hsa04216 | |||
Apoptosis | hsa04210 | ||||
Necroptosis | hsa04217 | ||||
Cell Process | Cell ferroptosis | ||||
Cell apoptosis | |||||
Cell necroptosis | |||||
In Vitro Model | HeLa cells | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 | |
SH-SY5Y cells | Neuroblastoma | Homo sapiens | CVCL_0019 | ||
NCI-H446 cells | Lung small cell carcinoma | Homo sapiens | CVCL_1562 | ||
Response regulation | Gallic acid (GA) could induce coexistence of multiple types of cell death pathways, including apoptosis characterized by mitochondrial cytochromecrelease and caspase-3 activation, ferroptosis characterized by lipid peroxidation, and necroptosis characterized by the loss of plasma membrane integrity in endocervical adenocarcinoma condition. | ||||
Experiment 2 Reporting the Ferroptosis-centered Disease Response by This Target | [10] | ||||
Responsed Disease | Cervical cancer [ICD-11: 2C77.Z] | ||||
Responsed Regulator | M-phase inducer phosphatase 1 (CDC25A) | Suppressor | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Autophagy | hsa04140 | ||||
Cell Process | Cell ferroptosis | ||||
Cell autophagy | |||||
In Vitro Model | SiHa cells | Cervical squamous cell carcinoma | Homo sapiens | CVCL_0032 | |
Ca Ski cells | Cervical squamous cell carcinoma | Homo sapiens | CVCL_1100 | ||
In Vivo Model |
Four-week-old male nude mice (N = 72) were purchased from SJA Laboratory Animal Co., Ltd. (Hunan, China), and raised in the standard animal facility room. Cervical cancer cells were infected with the control vector, Cdc25A, Cdc25A + sh-NC, and Cdc25A + sh-ErbB2 lentiviruses for 24 h and then unilateral subaxillary subcutaneously injected into nude mice (1 x 107 cells per mouse) to induce tumours.
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Response regulation | Cdc25A suppressed autophagy-dependent ferroptosis in cervical cancer cells by upregulating ErbB2 levels through the dephosphorylation of PKM2. These studies revealed that Cdc25A/PKM2/ErbB2 pathway-regulated ferroptosis could serve as a therapeutic target in cervical cancer. | ||||
Experiment 3 Reporting the Ferroptosis-centered Disease Response by This Target | [10] | ||||
Responsed Disease | Cervical cancer [ICD-11: 2C77.Z] | ||||
Responsed Regulator | Receptor tyrosine-protein kinase erbB-2 (ERBB2) | Suppressor | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Autophagy | hsa04140 | ||||
Cell Process | Cell ferroptosis | ||||
Cell autophagy | |||||
In Vitro Model | SiHa cells | Cervical squamous cell carcinoma | Homo sapiens | CVCL_0032 | |
Ca Ski cells | Cervical squamous cell carcinoma | Homo sapiens | CVCL_1100 | ||
In Vivo Model |
Four-week-old male nude mice (N = 72) were purchased from SJA Laboratory Animal Co., Ltd. (Hunan, China), and raised in the standard animal facility room. Cervical cancer cells were infected with the control vector, Cdc25A, Cdc25A + sh-NC, and Cdc25A + sh-ErbB2 lentiviruses for 24 h and then unilateral subaxillary subcutaneously injected into nude mice (1 x 107 cells per mouse) to induce tumours.
Click to Show/Hide
|
||||
Response regulation | Cdc25A suppressed autophagy-dependent ferroptosis in cervical cancer cells by upregulating ErbB2 levels through the dephosphorylation of PKM2. These studies revealed that Cdc25A/PKM2/ErbB2 pathway-regulated ferroptosis could serve as a therapeutic target in cervical cancer. | ||||
References