General Information of the m6A Target Gene (ID: M6ATAR00742)
Target Name LINC00902 (TUSC7)
Synonyms
LINC00902; LOC285194; NCRNA00295; LSAMP-AS3; non-protein coding RNA 295; LSAMP antisense RNA 3; tumor suppressor candidate 7 (non-protein coding)
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Gene Name TUSC7
Chromosomal Location 3q13.31
Gene ID 285194
HGNC ID
HGNC:27701
Ensembl Gene ID
ENSG00000243197
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.
References
Ref 1 M6A associated TSUC7 inhibition contributed to Erlotinib resistance in lung adenocarcinoma through a notch signaling activation dependent way. J Exp Clin Cancer Res. 2021 Oct 16;40(1):325. doi: 10.1186/s13046-021-02137-9.