General Information of the Ferroptosis Regulator (ID: REG20148)
Regulator Name hsa-miR-4291 (miRNA)
Synonyms
hsa-miR-4291
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Gene Name hsa-miR-4291
Regulator Type miRNA
MiRBase ID MIMAT0016922
Sequence
UUCAGCAGGAACAGCU

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Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
hsa-miR-4291 can regulate the following target(s), and cause disease/drug response(s). You can browse detail information of target(s) or disease/drug response(s).
Browse Target
Browse Disease
Long-chain-fatty-acid--CoA ligase 4 (ACSL4) [Driver]
In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator [1]
Target for Ferroptosis Driver
Responsed Disease Cervical cancer ICD-11: 2C77
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.
Cervical cancer [ICD-11: 2C77]
In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator hsa-miR-4291 (miRNA) miRNA
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.
References
Ref 1 Circular RNA circLMO1 Suppresses Cervical Cancer Growth and Metastasis by Triggering miR-4291/ACSL4-Mediated Ferroptosis. Front Oncol. 2022 Mar 7;12:858598. doi: 10.3389/fonc.2022.858598. eCollection 2022.