Ferroptosis-centered Disease Response Information

General Information of the Disease (ID: DIS00015)
Name
Mature T-cell lymphoma
ICD
ICD-11: 2A90
Full List of Target(s) of This Ferroptosis-centered Disease
Unspecific Target
In total 2 item(s) under this target
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target [1]
Responsed Disease T-cell acute lymphoblastic leukemia [ICD-11: 2A90]
Responsed Drug Hydnocarpin D Investigative
 Drug Info 
Responsed Regulator Microtubule-associated proteins 1A/1B light chain 3B {ECO:0000305} (MAP1LC3B) Driver
 Regulator 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-centered Disease Response by This Target [2]
Responsed Disease T-cell acute lymphoblastic leukemia [ICD-11: 2A90]
Responsed Drug Poricoic acid A Investigative
 Drug Info 
Pathway Response Ferroptosis hsa04216
Apoptosis hsa04210
Autophagy hsa04140
Cell Process Cell ferroptosis
Cell apoptosis
Cell autophagy
Cell proliferation
In Vitro Model Jurkat cells T acute lymphoblastic leukemia Homo sapiens CVCL_0065
MOLT-3 cells T-lymphoblastic leukemia Homo sapiens CVCL_0624
RPMI-8402 cells Acute lymphoblastic leukemia Homo sapiens CVCL_1667
RAW 264.7 cells Leukemia Mus musculus CVCL_0493
HK-2 cells Normal Homo sapiens CVCL_0302
CAM191 cells Normal Homo sapiens CVCL_BS93
L-02 cells Endocervical adenocarcinoma Homo sapiens CVCL_6926
In Vivo Model
BALB/c Nude Mice (4-6 weeks old) were purchased from Shanghai Experimental Animal Center of the Chinese Academy of Sciences (Shanghai, China) and then subcutaneously injection with JURKAT cells (1 x 107) suspended in 100 uL PBS. Tumor volume was measured once a week with a caliper according to the formula: 1/2 x length x width2. After tumors reached 100-200 mm3(at day 4), the mice were randomly assigned to three groups: the Control group, low dose of PAA (5 mg/kg) and high dose of PAA (10 mg/kg). PAA was administered through i.p. injection once a day at 5 or 10 mg/kg body weight. Mice in normal control group were given equal amounts of vehicle (saline). Body weights of mice were measured once a week during PAA treatments. After 4 weeks, blood samples were collected from each group of mice, and tumor tissues were removed and weighed for further analysis.

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Response regulation Poricoic acid A could significantly inhibit T-cell acute lymphoblastic leukemia (T-ALL) progression by inducing G2/M phase, apoptosis, mitochondrial dysfunction, ROS generation, autophagy and ferroptosis without detectable side effects both in vitro and in vivo.
References
Ref 1 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 2 Poricoic acid A (PAA) inhibits T-cell acute lymphoblastic leukemia through inducing autophagic cell death and ferroptosis. Biochem Biophys Res Commun. 2022 Jun 11;608:108-115. doi: 10.1016/j.bbrc.2022.03.105. Epub 2022 Mar 23.