Dataset Information

STING promotes proliferation and induces drug resistance in colorectal cancer by regulating the AMPK-mTOR pathway.

ABSTRACT:

Background

In recent years, reports regarding stimulator of interferon genes (STING) and the progression of colorectal cancer (CRC) have emerged rapidly, yet their association remains controversial. This research was aimed to provide an insight into the prognostic biomarker and therapeutic target significance of STING in CRC.

Methods

CRC Cell lines of HCT116 and SW480, as well as 32 paired CRC specimens were chosen for this study. STING expressions were examined by immunohistochemistry to evaluate the correlation with clinicopathological factors. Data analysis of STING expressions in colon cancer and rectal cancer were performed using The Cancer Genome Atlas (TCGA) database. siRNA was transfected into cell lines for knocking down the expression of STING. Transwell assay was employed to evaluate cell migration and invasiveness. CCK-8 assay was used for assessing the change of cell proliferation. Drug sensitive test was involved to evaluate drug resistance of cell lines. Gene Set Enrichment Analysis (GSEA) was applied for exploring potential downstream mechanism of STING in CRC progression and Western blotting is used for mechanism validation.

Results

In the thirty-two paired CRC and adjacent normal tissues, we found a significant up-regulated in STING expression with immunohistochemical staining in cancer tissues compared with adjacent normal tissues (P<0.01), which was correlated with the tumor-node-metastasis (TNM) stage of patients (P=0.028). Meanwhile, GESA enrichment analysis indicated a remarkable change in mTOR signaling following STING regulation. In HCT116 and SW480 cell lines of CRC, When STING was down-regulated, its biological behavior of cell viability, cell invasion and drug sensitivity to 5-fluorouracil were significantly reduced (P<0.05), we also observed the up-regulation of P-AMPK (P<0.05) and down-regulation of p-mTOR (P<0.05).

Conclusions

STING expressions was significantly up-regulated in CRC tissues. Expression of STING was correlated with the TNM stage of patients. STING is found to promote cell proliferation, invasion ability and drug resistance mediating AMPK-mTOR signaling in CRC. STING could be a promising target for the sensitization of chemotherapy and inhibits CRC progression.

SUBMITTER: Yao H

PROVIDER: S-EPMC9660059 | biostudies-literature | 2022 Oct

REPOSITORIES: biostudies-literature

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Publications

STING promotes proliferation and induces drug resistance in colorectal cancer by regulating the AMPK-mTOR pathway.

Yao Huihui H Wang Suo S Zhou Xin X Sun Jinbing J Zhou Guoqiang G Zhou Diyuan D Chen Guoliang G Shi Xinyu X Chen Junjie J Shi Bo B Tai Qingliang Q Mi Xiuwei X Sun Liang L Yao Yizhou Y He Songbing S

Journal of gastrointestinal oncology 20221001 5

<h4>Background</h4>In recent years, reports regarding stimulator of interferon genes (STING) and the progression of colorectal cancer (CRC) have emerged rapidly, yet their association remains controversial. This research was aimed to provide an insight into the prognostic biomarker and therapeutic target significance of STING in CRC.<h4>Methods</h4>CRC Cell lines of HCT116 and SW480, as well as 32 paired CRC specimens were chosen for this study. STING expressions were examined by immunohistochem ...[more]

PMID: 36388670

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Dataset Information

STING promotes proliferation and induces drug resistance in colorectal cancer by regulating the AMPK-mTOR pathway.

Background

Methods

Results

Conclusions

Publications

STING promotes proliferation and induces drug resistance in colorectal cancer by regulating the AMPK-mTOR pathway.

Similar Datasets

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