Ferroptosis Regulator Information

General Information of the Ferroptosis Regulator (ID: REG10391)

Regulator Name	Microtubule-associated proteins 1A/1B light chain 3B {ECO:0000305} (MAP1LC3B)
Synonyms	MAP1ALC3; Autophagy-related protein LC3 B; Autophagy-related ubiquitin-like modifier LC3 B; MAP1 light chain 3-like protein 2; MAP1A/MAP1B light chain 3 B; Microtubule-associated protein 1 light chain 3 beta Click to Show/Hide
Gene Name	MAP1LC3B
Gene ID	81631
Regulator Type	Protein coding
Uniprot ID	Q9GZQ8
Sequence	MPSEKTFKQRRTFEQRVEDVRLIREQHPTKIPVIIERYKGEKQLPVLDKTKFLVPDHVNM SELIKIIRRRLQLNANQAFFLLVNGHSMVSVSTPISEVYESEKDEDGFLYMVYASQETFG MKLSV Click to Show/Hide
Family	ATG8 family
Function	Ubiquitin-like modifier involved in formation of autophagosomal vacuoles (autophagosomes). Plays a role in mitophagy which contributes to regulate mitochondrial quantity and quality by eliminating the mitochondria to a basal level to fulfill cellular energy requirements and preventing excess ROS production. In response to cellular stress and upon mitochondria fission, binds C-18 ceramides and anchors autophagolysosomes to outer mitochondrial membranes to eliminate damaged mitochondria. While LC3s are involved in elongation of the phagophore membrane, the GABARAP/GATE-16 subfamily is essential for a later stage in autophagosome maturation. Promotes primary ciliogenesis by removing OFD1 from centriolar satellites via the autophagic pathway. Through its interaction with the reticulophagy receptor TEX264, participates in the remodeling of subdomains of the endoplasmic reticulum into autophagosomes upon nutrient stress, which then fuse with lysosomes for endoplasmic reticulum turnover. Upon nutrient stress, directly recruits cofactor JMY to the phagophore membrane surfaces and promotes JMY's actin nucleation activity and autophagosome biogenesis during autophagy. { \| , \| , \| , \| , \| , \| , \| , \| }. Click to Show/Hide
HGNC ID	HGNC:13352
KEGG ID	hsa:81631

Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)

MAP1LC3B 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

Browse Drug

Ferritin heavy chain (FTH1) [Suppressor; Marker]

Target Info

In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator				[1]
Target for Ferroptosis	Marker/Suppressor
Responsed Disease	Glioblastoma		ICD-11: 2A00	Disease Info
Responsed Drug	Amentoflavone		Investigative	Drug Info
Pathway Response	mTOR signaling pathway			hsa04150
	Fatty acid metabolism			hsa01212
	Autophagy			hsa04140
Cell Process	Cell ferroptosis
	Cell autophagy
	Cell proliferation
In Vitro Model	U-251MG cells	Astrocytoma	Homo sapiens	CVCL_0021
	U-373MG cells	Astrocytoma	Homo sapiens	CVCL_2219
In Vivo Model	1 x 10⁷ U251 cells were subcutaneously injected into the right back of the four-week-old BALB/c nude mice. After the tumor grown to 100 mm³, mice were randomly divided into 3 groups: mice in control group receivedintraperitoneal injectionof saline, while mice in AF treatment group received intraperitoneal injection at dosages of 40 mg/kg/day or 80 mg/kg/day, respectively. Click to Show/Hide
Response regulation	Amentoflavone (AF) triggered ferroptosis in autophagy-dependent manner. Furthermore, the expression of LC3B, Beclin1, ATG5, ATG7 were increased, and the expression of FTH were decreased by AF in a dose-dependent manner in vivo. AF has the potential to be considered as a novel treatment agent in glioma.

Unspecific Target [Unspecific Target]

In total 4 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator				[2]
Responsed Disease	Mature T-cell lymphoma		ICD-11: 2A90	Disease Info
Responsed Drug	Hydnocarpin D		Investigative	Drug Info
Pathway Response	Ferroptosis			hsa04216
	Autophagy			hsa04140
	Apoptosis			hsa04210
Cell Process	Cell ferroptosis
	Cell autophagy
	Cell apoptosis
In Vitro Model	Jurkat cells	T acute lymphoblastic leukemia	Homo sapiens	CVCL_0065
	MOLT4 cells	Adult T acute lymphoblastic leukemia	Homo sapiens	CVCL_0013
	CAM191 cells	Normal	Homo sapiens	CVCL_BS93
Response regulation	Using T cell acute lymphoblastic leukemia (T-ALL) cell lines Jurkat and Molt-4 as model system, Hydnocarpin D (HD) suppressed T-ALL proliferationin vitro, via induction of cell cycle arrest and subsequent apoptosis. Furthermore, HD increased the MAP1LC3B (LC3-II) levels and the formation of autophagolysosome vacuoles, both of which are markers for autophagy.
Experiment 2 Reporting the Ferroptosis Target of This Regulator				[3]
Responsed Disease	Gastric cancer		ICD-11: 2B72	Disease Info
Responsed Drug	Polyphyllin B		Investigative	Drug Info
Pathway Response	Ferroptosis			hsa04216
Cell Process	Cell ferroptosis
	Cell apoptosis
	Cell proliferation
In Vitro Model	NUGC-3 cells	Gastric carcinoma	Homo sapiens	CVCL_1612
	MKN-1 cells	Gastric carcinoma	Homo sapiens	CVCL_1415
	MKN45 cells	Gastric adenocarcinoma	Homo sapiens	CVCL_0434
	HGC-27 cells	Gastric carcinoma	Homo sapiens	CVCL_1279
	NUGC-4 cells	Gastric signet ring cell adenocarcinoma	Homo sapiens	CVCL_3082
In Vivo Model	The nude mice were raised in our laboratory for a week before the experiment. Then, 5 x 10⁶ MKN-1 cells were subcutaneously injected to establish the subcutaneous xenograft tumour model in nude mice. When the maximum diameter of the xenograft tumours grew steadily to 1 cm, they were dissected completely and cut into 1 mm³ tissue fragments. Then, the tissue fragment was inserted into the surface of the serosa on the greater curvature of the stomach. Different doses of PB (2.5 mg/kg or 5.0 mg/kg) were given by intraperitoneal injection once a day for 3 weeks. The control group was given the same volume of vehicle. The positive control group was given 5-Fu at the dose of 10 mg/kg. The body weight and tumour size of nude mice were recorded. Mice were administered fluorescein substrate (150 mg/kg) intraperitoneally for in vivo imaging twice a week on a Xenogen IVIS 200 imaging system (Caliper Life Sciences, USA). The tumour inhibition rate was analysed using LT Living Image 4.3 Software. Click to Show/Hide
Response regulation	We identified a novel GPx4 inhibitor, polyphyllin B (PB), which can induce ferroptosis by down-regulating GPx4 expression in gastric cancer cells. It has also been shown to inhibit cell proliferation, suppress invasion and migration, induce apoptosis, and block the cell cycle progression in GC cellsin vitro. Then, immunofluorescence and western blotting assay confirmed that PB can regulate the expression of LC3B, TFR1, NOCA4 and FTH1in vitro, which suggested that suggest that PB may increase the level of Fe2+by transporting Fe3+into the cell by TFR1 and promoting NCOA4-dependent iron autophagy.
Experiment 3 Reporting the Ferroptosis Target of This Regulator				[4]
Responsed Disease	Hereditary Leiomyomatosis		ICD-11: 2C90	Disease Info
Responsed Drug	Sodium arsenite		Investigative	Drug Info
Pathway Response	Fatty acid metabolism			hsa01212
	Ferroptosis			hsa04216
	Autophagy			hsa04140
Cell Process	Cell ferroptosis
	Cell autophagy
In Vitro Model	PC12 cells	Adrenal gland pheochromocytoma	Rattus norvegicus	CVCL_0481
In Vivo Model	A total of thirty-two healthy specificpathogenfree C57BL/6J male mice at seven weeks of age and weighted 20-24 g were purchased from the Experimental Animal Center of Chongqing Medical University. After administration of arsenite via drinking water, the animals were euthanized by pentobarbital sodium, three of the animals were subjected to the perfusion fixation, and subsequently, the hippocampus tissues were rapidly dissected on ice and immersed into 4% paraformaldehyde for pre-fixation. Click to Show/Hide
Response regulation	Arsenite was able to trigger ferroptosis in the adrenal gland pheochromocytoma cells. Arsenite significantly decreased the expressions of ferritin and NCOA4, but sharply enhanced the level of autophagy marker LC3B, suggesting the activation of ferritinophagy by arsenite.
Experiment 4 Reporting the Ferroptosis Target of This Regulator				[5]
Responsed Disease	Traumatic brain injury		ICD-11: NA07	Disease Info
Responsed Drug	Baicalin		Terminated	Drug Info
Pathway Response	Ferroptosis			hsa04216
Cell Process	Cell ferroptosis
	Cell autophagy
	Cell apoptosis
In Vitro Model	rPNs (Rat primary neurons)
In Vivo Model	Rats were injected with 4 mL/kg of chloral hydrate for anesthesia and then put on a stereotactic apparatus. Subsequently, the needle was tilted at 55 in the sagittal plane and fixed anterior to the bregma (7.5 mm). The needle tip was toward the right and lowered the anterior to the chiasma (2 mm). Finally, the nonheparinized autologous femoral arterial blood (0.3 mL) was injected into a prechiasmatic cistern using a syringe pump. Rat temperature was maintained at 37 ± 0.5 during the surgery. The rats in the sham group were injected with the same dose of saline into a prechiasmatic cistern. At last, rats were monitored for recovery and then returned to cages. Click to Show/Hide
Response regulation	Baicalin was confirmed to suppress the beclin1, LC3-II, and LC3-I protein levels in rat brain tissues. Moreover, we found that baicalin inhibited neuronal apoptosis. Overall, baicalin suppressed autophagy-dependent ferroptosis in early brain injury after subarachnoid hemorrhage.

Glioblastoma [ICD-11: 2A00]

Disease Info

In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response				[1]
Target Regulator	Microtubule-associated proteins 1A/1B light chain 3B {ECO:0000305} (MAP1LC3B)		Protein coding	Regulator Info
Responsed Drug	Amentoflavone		Investigative	Drug Info
Pathway Response	mTOR signaling pathway			hsa04150
	Fatty acid metabolism			hsa01212
	Autophagy			hsa04140
Cell Process	Cell ferroptosis
	Cell autophagy
	Cell proliferation
In Vitro Model	U-251MG cells	Astrocytoma	Homo sapiens	CVCL_0021
	U-373MG cells	Astrocytoma	Homo sapiens	CVCL_2219
In Vivo Model	1 x 10⁷ U251 cells were subcutaneously injected into the right back of the four-week-old BALB/c nude mice. After the tumor grown to 100 mm³, mice were randomly divided into 3 groups: mice in control group receivedintraperitoneal injectionof saline, while mice in AF treatment group received intraperitoneal injection at dosages of 40 mg/kg/day or 80 mg/kg/day, respectively. Click to Show/Hide
Response regulation	Amentoflavone (AF) triggered ferroptosis in autophagy-dependent manner. Furthermore, the expression of LC3B, Beclin1, ATG5, ATG7 were increased, and the expression of FTH were decreased by AF in a dose-dependent manner in vivo. AF has the potential to be considered as a novel treatment agent in glioma.

Mature T-cell lymphoma [ICD-11: 2A90]

Disease Info

In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response				[2]
Target Regulator	Microtubule-associated proteins 1A/1B light chain 3B {ECO:0000305} (MAP1LC3B)		Protein coding	Regulator Info
Responsed Drug	Hydnocarpin D		Investigative	Drug Info
Pathway Response	Ferroptosis			hsa04216
	Autophagy			hsa04140
	Apoptosis			hsa04210
Cell Process	Cell ferroptosis
	Cell autophagy
	Cell apoptosis
In Vitro Model	Jurkat cells	T acute lymphoblastic leukemia	Homo sapiens	CVCL_0065
	MOLT4 cells	Adult T acute lymphoblastic leukemia	Homo sapiens	CVCL_0013
	CAM191 cells	Normal	Homo sapiens	CVCL_BS93
Response regulation	Using T cell acute lymphoblastic leukemia (T-ALL) cell lines Jurkat and Molt-4 as model system, Hydnocarpin D (HD) suppressed T-ALL proliferationin vitro, via induction of cell cycle arrest and subsequent apoptosis. Furthermore, HD increased the MAP1LC3B (LC3-II) levels and the formation of autophagolysosome vacuoles, both of which are markers for autophagy.

Gastric cancer [ICD-11: 2B72]

Disease Info

In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response				[3]
Target Regulator	Microtubule-associated proteins 1A/1B light chain 3B {ECO:0000305} (MAP1LC3B)		Protein coding	Regulator Info
Responsed Drug	Polyphyllin B		Investigative	Drug Info
Pathway Response	Ferroptosis			hsa04216
Cell Process	Cell ferroptosis
	Cell apoptosis
	Cell proliferation
In Vitro Model	NUGC-3 cells	Gastric carcinoma	Homo sapiens	CVCL_1612
	MKN-1 cells	Gastric carcinoma	Homo sapiens	CVCL_1415
	MKN45 cells	Gastric adenocarcinoma	Homo sapiens	CVCL_0434
	HGC-27 cells	Gastric carcinoma	Homo sapiens	CVCL_1279
	NUGC-4 cells	Gastric signet ring cell adenocarcinoma	Homo sapiens	CVCL_3082
In Vivo Model	The nude mice were raised in our laboratory for a week before the experiment. Then, 5 x 10⁶ MKN-1 cells were subcutaneously injected to establish the subcutaneous xenograft tumour model in nude mice. When the maximum diameter of the xenograft tumours grew steadily to 1 cm, they were dissected completely and cut into 1 mm³ tissue fragments. Then, the tissue fragment was inserted into the surface of the serosa on the greater curvature of the stomach. Different doses of PB (2.5 mg/kg or 5.0 mg/kg) were given by intraperitoneal injection once a day for 3 weeks. The control group was given the same volume of vehicle. The positive control group was given 5-Fu at the dose of 10 mg/kg. The body weight and tumour size of nude mice were recorded. Mice were administered fluorescein substrate (150 mg/kg) intraperitoneally for in vivo imaging twice a week on a Xenogen IVIS 200 imaging system (Caliper Life Sciences, USA). The tumour inhibition rate was analysed using LT Living Image 4.3 Software. Click to Show/Hide
Response regulation	We identified a novel GPx4 inhibitor, polyphyllin B (PB), which can induce ferroptosis by down-regulating GPx4 expression in gastric cancer cells. It has also been shown to inhibit cell proliferation, suppress invasion and migration, induce apoptosis, and block the cell cycle progression in GC cellsin vitro. Then, immunofluorescence and western blotting assay confirmed that PB can regulate the expression of LC3B, TFR1, NOCA4 and FTH1in vitro, which suggested that suggest that PB may increase the level of Fe2+by transporting Fe3+into the cell by TFR1 and promoting NCOA4-dependent iron autophagy.

Hereditary Leiomyomatosis [ICD-11: 2C90]

Disease Info

In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response				[4]
Target Regulator	Microtubule-associated proteins 1A/1B light chain 3B {ECO:0000305} (MAP1LC3B)		Protein coding	Regulator Info
Responsed Drug	Sodium arsenite		Investigative	Drug Info
Pathway Response	Fatty acid metabolism			hsa01212
	Ferroptosis			hsa04216
	Autophagy			hsa04140
Cell Process	Cell ferroptosis
	Cell autophagy
In Vitro Model	PC12 cells	Adrenal gland pheochromocytoma	Rattus norvegicus	CVCL_0481
In Vivo Model	A total of thirty-two healthy specificpathogenfree C57BL/6J male mice at seven weeks of age and weighted 20-24 g were purchased from the Experimental Animal Center of Chongqing Medical University. After administration of arsenite via drinking water, the animals were euthanized by pentobarbital sodium, three of the animals were subjected to the perfusion fixation, and subsequently, the hippocampus tissues were rapidly dissected on ice and immersed into 4% paraformaldehyde for pre-fixation. Click to Show/Hide
Response regulation	Arsenite was able to trigger ferroptosis in the adrenal gland pheochromocytoma cells. Arsenite significantly decreased the expressions of ferritin and NCOA4, but sharply enhanced the level of autophagy marker LC3B, suggesting the activation of ferritinophagy by arsenite.

Traumatic brain injury [ICD-11: NA07]

Disease Info

In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response			[5]
Target Regulator	Microtubule-associated proteins 1A/1B light chain 3B {ECO:0000305} (MAP1LC3B)	Protein coding	Regulator Info
Responsed Drug	Baicalin	Terminated	Drug Info
Pathway Response	Ferroptosis		hsa04216
Cell Process	Cell ferroptosis
	Cell autophagy
	Cell apoptosis
In Vitro Model	rPNs (Rat primary neurons)
In Vivo Model	Rats were injected with 4 mL/kg of chloral hydrate for anesthesia and then put on a stereotactic apparatus. Subsequently, the needle was tilted at 55 in the sagittal plane and fixed anterior to the bregma (7.5 mm). The needle tip was toward the right and lowered the anterior to the chiasma (2 mm). Finally, the nonheparinized autologous femoral arterial blood (0.3 mL) was injected into a prechiasmatic cistern using a syringe pump. Rat temperature was maintained at 37 ± 0.5 during the surgery. The rats in the sham group were injected with the same dose of saline into a prechiasmatic cistern. At last, rats were monitored for recovery and then returned to cages. Click to Show/Hide
Response regulation	Baicalin was confirmed to suppress the beclin1, LC3-II, and LC3-I protein levels in rat brain tissues. Moreover, we found that baicalin inhibited neuronal apoptosis. Overall, baicalin suppressed autophagy-dependent ferroptosis in early brain injury after subarachnoid hemorrhage.

Amentoflavone [Investigative]

Drug Info

In total 1 item(s) under this drug
Experiment 1 Reporting the Ferroptosis-centered Drug Response				[1]
Drug for Ferroptosis	Inducer
Response Target	Ferritin heavy chain (FTH1)		Suppressor; Marker	Target Info
Responsed Disease	Glioblastoma		ICD-11: 2A00	Disease Info
Pathway Response	mTOR signaling pathway			hsa04150
	Fatty acid metabolism			hsa01212
	Autophagy			hsa04140
Cell Process	Cell ferroptosis
	Cell autophagy
	Cell proliferation
In Vitro Model	U-251MG cells	Astrocytoma	Homo sapiens	CVCL_0021
	U-373MG cells	Astrocytoma	Homo sapiens	CVCL_2219
In Vivo Model	1 x 10⁷ U251 cells were subcutaneously injected into the right back of the four-week-old BALB/c nude mice. After the tumor grown to 100 mm³, mice were randomly divided into 3 groups: mice in control group receivedintraperitoneal injectionof saline, while mice in AF treatment group received intraperitoneal injection at dosages of 40 mg/kg/day or 80 mg/kg/day, respectively. Click to Show/Hide
Response regulation	Amentoflavone (AF) triggered ferroptosis in autophagy-dependent manner. Furthermore, the expression of LC3B, Beclin1, ATG5, ATG7 were increased, and the expression of FTH were decreased by AF in a dose-dependent manner in vivo. AF has the potential to be considered as a novel treatment agent in glioma.

Baicalin [Terminated]

Drug Info

In total 1 item(s) under this drug
Experiment 1 Reporting the Ferroptosis-centered Drug Response			[5]
Drug for Ferroptosis	Suppressor
Response Target	Unspecific Target
Responsed Disease	Traumatic brain injury	ICD-11: NA07	Disease Info
Pathway Response	Ferroptosis		hsa04216
Cell Process	Cell ferroptosis
	Cell autophagy
	Cell apoptosis
In Vitro Model	rPNs (Rat primary neurons)
In Vivo Model	Rats were injected with 4 mL/kg of chloral hydrate for anesthesia and then put on a stereotactic apparatus. Subsequently, the needle was tilted at 55 in the sagittal plane and fixed anterior to the bregma (7.5 mm). The needle tip was toward the right and lowered the anterior to the chiasma (2 mm). Finally, the nonheparinized autologous femoral arterial blood (0.3 mL) was injected into a prechiasmatic cistern using a syringe pump. Rat temperature was maintained at 37 ± 0.5 during the surgery. The rats in the sham group were injected with the same dose of saline into a prechiasmatic cistern. At last, rats were monitored for recovery and then returned to cages. Click to Show/Hide
Response regulation	Baicalin was confirmed to suppress the beclin1, LC3-II, and LC3-I protein levels in rat brain tissues. Moreover, we found that baicalin inhibited neuronal apoptosis. Overall, baicalin suppressed autophagy-dependent ferroptosis in early brain injury after subarachnoid hemorrhage.

Hydnocarpin D [Investigative]

Drug Info

In total 1 item(s) under this drug
Experiment 1 Reporting the Ferroptosis-centered Drug Response				[2]
Drug for Ferroptosis	Inducer
Response Target	Unspecific Target
Responsed Disease	Mature T-cell lymphoma		ICD-11: 2A90	Disease Info
Pathway Response	Ferroptosis			hsa04216
	Autophagy			hsa04140
	Apoptosis			hsa04210
Cell Process	Cell ferroptosis
	Cell autophagy
	Cell apoptosis
In Vitro Model	Jurkat cells	T acute lymphoblastic leukemia	Homo sapiens	CVCL_0065
	MOLT4 cells	Adult T acute lymphoblastic leukemia	Homo sapiens	CVCL_0013
	CAM191 cells	Normal	Homo sapiens	CVCL_BS93
Response regulation	Using T cell acute lymphoblastic leukemia (T-ALL) cell lines Jurkat and Molt-4 as model system, Hydnocarpin D (HD) suppressed T-ALL proliferationin vitro, via induction of cell cycle arrest and subsequent apoptosis. Furthermore, HD increased the MAP1LC3B (LC3-II) levels and the formation of autophagolysosome vacuoles, both of which are markers for autophagy.

Polyphyllin B [Investigative]

Drug Info

In total 1 item(s) under this drug
Experiment 1 Reporting the Ferroptosis-centered Drug Response				[3]
Drug for Ferroptosis	Inducer
Response Target	Unspecific Target
Responsed Disease	Gastric cancer		ICD-11: 2B72	Disease Info
Pathway Response	Ferroptosis			hsa04216
Cell Process	Cell ferroptosis
	Cell apoptosis
	Cell proliferation
In Vitro Model	NUGC-3 cells	Gastric carcinoma	Homo sapiens	CVCL_1612
	MKN-1 cells	Gastric carcinoma	Homo sapiens	CVCL_1415
	MKN45 cells	Gastric adenocarcinoma	Homo sapiens	CVCL_0434
	HGC-27 cells	Gastric carcinoma	Homo sapiens	CVCL_1279
	NUGC-4 cells	Gastric signet ring cell adenocarcinoma	Homo sapiens	CVCL_3082
In Vivo Model	The nude mice were raised in our laboratory for a week before the experiment. Then, 5 x 10⁶ MKN-1 cells were subcutaneously injected to establish the subcutaneous xenograft tumour model in nude mice. When the maximum diameter of the xenograft tumours grew steadily to 1 cm, they were dissected completely and cut into 1 mm³ tissue fragments. Then, the tissue fragment was inserted into the surface of the serosa on the greater curvature of the stomach. Different doses of PB (2.5 mg/kg or 5.0 mg/kg) were given by intraperitoneal injection once a day for 3 weeks. The control group was given the same volume of vehicle. The positive control group was given 5-Fu at the dose of 10 mg/kg. The body weight and tumour size of nude mice were recorded. Mice were administered fluorescein substrate (150 mg/kg) intraperitoneally for in vivo imaging twice a week on a Xenogen IVIS 200 imaging system (Caliper Life Sciences, USA). The tumour inhibition rate was analysed using LT Living Image 4.3 Software. Click to Show/Hide
Response regulation	We identified a novel GPx4 inhibitor, polyphyllin B (PB), which can induce ferroptosis by down-regulating GPx4 expression in gastric cancer cells. It has also been shown to inhibit cell proliferation, suppress invasion and migration, induce apoptosis, and block the cell cycle progression in GC cellsin vitro. Then, immunofluorescence and western blotting assay confirmed that PB can regulate the expression of LC3B, TFR1, NOCA4 and FTH1in vitro, which suggested that suggest that PB may increase the level of Fe2+by transporting Fe3+into the cell by TFR1 and promoting NCOA4-dependent iron autophagy.

Sodium arsenite [Investigative]

Drug Info

In total 1 item(s) under this drug
Experiment 1 Reporting the Ferroptosis-centered Drug Response				[4]
Drug for Ferroptosis	Inducer
Response Target	Unspecific Target
Responsed Disease	Hereditary Leiomyomatosis		ICD-11: 2C90	Disease Info
Pathway Response	Fatty acid metabolism			hsa01212
	Ferroptosis			hsa04216
	Autophagy			hsa04140
Cell Process	Cell ferroptosis
	Cell autophagy
In Vitro Model	PC12 cells	Adrenal gland pheochromocytoma	Rattus norvegicus	CVCL_0481
In Vivo Model	A total of thirty-two healthy specificpathogenfree C57BL/6J male mice at seven weeks of age and weighted 20-24 g were purchased from the Experimental Animal Center of Chongqing Medical University. After administration of arsenite via drinking water, the animals were euthanized by pentobarbital sodium, three of the animals were subjected to the perfusion fixation, and subsequently, the hippocampus tissues were rapidly dissected on ice and immersed into 4% paraformaldehyde for pre-fixation. Click to Show/Hide
Response regulation	Arsenite was able to trigger ferroptosis in the adrenal gland pheochromocytoma cells. Arsenite significantly decreased the expressions of ferritin and NCOA4, but sharply enhanced the level of autophagy marker LC3B, suggesting the activation of ferritinophagy by arsenite.

References

Ref 1	Amentoflavone suppresses cell proliferation and induces cell death through triggering autophagy-dependent ferroptosis in human glioma. Life Sci. 2020 Apr 15;247:117425. doi: 10.1016/j.lfs.2020.117425. Epub 2020 Feb 11.
Ref 2	Inhibitory effect of hydnocarpin D on T-cell acute lymphoblastic leukemia via induction of autophagy-dependent ferroptosis. Exp Biol Med (Maywood). 2021 Jul;246(13):1541-1553. doi: 10.1177/15353702211004870. Epub 2021 Apr 29.
Ref 3	Polyphyllin B Suppresses Gastric Tumor Growth by Modulating Iron Metabolism and Inducing Ferroptosis. Int J Biol Sci. 2023 Jan 31;19(4):1063-1079. doi: 10.7150/ijbs.80324. eCollection 2023.
Ref 4	Arsenite induces ferroptosis in the neuronal cells via activation of ferritinophagy. Food Chem Toxicol. 2021 May;151:112114. doi: 10.1016/j.fct.2021.112114. Epub 2021 Mar 13.
Ref 5	Baicalin suppresses autophagy-dependent ferroptosis in early brain injury after subarachnoid hemorrhage. Bioengineered. 2021 Dec;12(1):7794-7804. doi: 10.1080/21655979.2021.1975999.

Ferroptosis Regulator Information

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Correspondence

Prof. Shuiping Liu