m6A Target Gene Information
General Information of the m6A Target Gene (ID: M6ATAR00742)
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
TUSC7
can be regulated by the following regulator(s), and cause disease/drug response(s). You can browse detail information of regulator(s) or disease/drug response(s).
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YTH domain-containing family protein 2 (YTHDF2) [READER]
In total 1 item(s) under this regulator | ||||
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene | [1] | |||
Response Summary | In lung adenocarcinoma, The miR-146a/Notch signaling was sustained highly activated in a m6A dependent manner, and the m6A regulator of YTHDF2 suppressed LINC00902 (TUSC7), both of which contributed to the resistant features. Functionally, the sponge type of TUSC7 regulation of miR-146a inhibited Notch signaling functions, and affected the cancer progression and stem cells' renewal in Erlotinib resistant PC9 cells (PC9ER) and Erlotinib resistant HCC827 cells (HCC827ER) cells. | |||
Target Regulation | Down regulation | |||
Responsed Disease | Lung adenocarcinoma | ICD-11: 2C25.0 | ||
Responsed Drug | Erlotinib | Approved | ||
Pathway Response | Notch signaling pathway | hsa04330), EGFR tyrosine kinase inhibitor resistance | ||
In-vitro Model | PC-9 | Lung adenocarcinoma | Homo sapiens | CVCL_B260 |
HEK293T | Normal | Homo sapiens | CVCL_0063 | |
HCC827 | Lung adenocarcinoma | Homo sapiens | CVCL_2063 | |
In-vivo Model | Control vector, TUSC7 knockout, FLI-06 treated H1975 cells (1*107) cells were suspended in 100 uL of serum-free DMEM medium (Hyclone, USA), mixed with matrix gel (Corning, USA), and then were injected subcutaneously. The changes in the tumor size were recorded every 3 or 5 days. | |||
Lung cancer [ICD-11: 2C25]
In total 1 item(s) under this disease | ||||
Experiment 1 Reporting the m6A-centered Disease Response | [1] | |||
Response Summary | In lung adenocarcinoma, The miR-146a/Notch signaling was sustained highly activated in a m6A dependent manner, and the m6A regulator of YTHDF2 suppressed LINC00902 (TUSC7), both of which contributed to the resistant features. Functionally, the sponge type of TUSC7 regulation of miR-146a inhibited Notch signaling functions, and affected the cancer progression and stem cells' renewal in Erlotinib resistant PC9 cells (PC9ER) and Erlotinib resistant HCC827 cells (HCC827ER) cells. | |||
Responsed Disease | Lung adenocarcinoma [ICD-11: 2C25.0] | |||
Target Regulator | YTH domain-containing family protein 2 (YTHDF2) | READER | ||
Target Regulation | Down regulation | |||
Responsed Drug | Erlotinib | Approved | ||
Pathway Response | Notch signaling pathway | hsa04330), EGFR tyrosine kinase inhibitor resistance | ||
In-vitro Model | PC-9 | Lung adenocarcinoma | Homo sapiens | CVCL_B260 |
HEK293T | Normal | Homo sapiens | CVCL_0063 | |
HCC827 | Lung adenocarcinoma | Homo sapiens | CVCL_2063 | |
In-vivo Model | Control vector, TUSC7 knockout, FLI-06 treated H1975 cells (1*107) cells were suspended in 100 uL of serum-free DMEM medium (Hyclone, USA), mixed with matrix gel (Corning, USA), and then were injected subcutaneously. The changes in the tumor size were recorded every 3 or 5 days. | |||
Erlotinib
[Approved]
In total 1 item(s) under this drug | ||||
Experiment 1 Reporting the m6A-centered Drug Response | [1] | |||
Response Summary | In lung adenocarcinoma, The miR-146a/Notch signaling was sustained highly activated in a m6A dependent manner, and the m6A regulator of YTHDF2 suppressed LINC00902 (TUSC7), both of which contributed to the resistant features. Functionally, the sponge type of TUSC7 regulation of miR-146a inhibited Notch signaling functions, and affected the cancer progression and stem cells' renewal in Erlotinib resistant PC9 cells (PC9ER) and Erlotinib resistant HCC827 cells (HCC827ER) cells. | |||
Target Regulator | YTH domain-containing family protein 2 (YTHDF2) | READER | ||
Target Regulation | Down regulation | |||
Responsed Disease | Lung adenocarcinoma | ICD-11: 2C25.0 | ||
Pathway Response | Notch signaling pathway | hsa04330), EGFR tyrosine kinase inhibitor resistance | ||
In-vitro Model | PC-9 | Lung adenocarcinoma | Homo sapiens | CVCL_B260 |
HEK293T | Normal | Homo sapiens | CVCL_0063 | |
HCC827 | Lung adenocarcinoma | Homo sapiens | CVCL_2063 | |
In-vivo Model | Control vector, TUSC7 knockout, FLI-06 treated H1975 cells (1*107) cells were suspended in 100 uL of serum-free DMEM medium (Hyclone, USA), mixed with matrix gel (Corning, USA), and then were injected subcutaneously. The changes in the tumor size were recorded every 3 or 5 days. | |||