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Long noncoding RNA SNHG6 silencing sensitized esophageal cancer cells to 5-FU via EZH2/STAT pathway
Ran Tan1, Jia Liu2, Jiang Wang3
1Department of Clinical Pharmacy, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou, China.
Abstract:
Chemotherapy was the main treatment method for esophageal cancer (EC) patients. However, chemotherapy resistance due to multiple factors is a major barrier to EC treatment. For investigating how small nucleolar RNA host gene 6 (SNHG6) affected the 5-fluorouracil (5-FU) resistance in EC as well as its possible molecular mechanism. This work conducted cell viability assay, clone formation, scratch assays together with cell apoptosis for evaluating the roles of SNHG6 and enhancer of zeste homolog 2 (EZH2, the histone-lysine N-methyltransferase). Relevant molecular mechanism was identified by RT-qPCR analysis together with Western-blot (WB) assays. Our data showed that SNHG6 expression increased in EC cells. SNHG6 promotes colony formation and migration, whereas suppresses EC cell apoptosis. SNHG6 silencing markedly promoted 5-FU-mediated suppression on KYSE150 and KYSE450 cells. Additional mechanism studies showed that SNHG6 modulating STAT3 and H3K27me3 via promoting EZH2 level. Similar to the function of SNHG6, abnormal expression of EZH2 promotes the malignancy of EC and intensifies its resistance to 5-FU. In addition, overexpression of EZH2 abolished the role of SNHG6 silencing in 5-FU sensitivity in EC cells. SNHG6 overexpression promoted malignancy of EC and increased EC cell resistance to 5-FU. Besides, further molecular mechanism studies provided a novel regulatory pathways that SNHG6 knockdown promoted EC cell sensitivity to 5-FU by modulating STAT3 and H3K27me3 via promoting EZH2 expression.
Insights
Small nucleolar RNA host gene 6 (SNHG6) promotes esophageal cancer (EC) malignancy and 5-fluorouracil (5-FU) resistance by increasing enhancer of zeste homolog 2 (EZH2) levels. Silencing SNHG6 enhances 5-FU sensitivity in EC cells.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- Chemotherapy resistance is a significant challenge in esophageal cancer (EC) treatment.
- Small nucleolar RNA host gene 6 (SNHG6) is implicated in various cancers, but its role in EC chemotherapy resistance requires elucidation.
Purpose of the Study:
- To investigate the effect of SNHG6 on 5-fluorouracil (5-FU) resistance in EC.
- To explore the underlying molecular mechanisms involving enhancer of zeste homolog 2 (EZH2), STAT3, and H3K27me3.
Main Methods:
- Cell viability, clone formation, scratch, and apoptosis assays were performed.
- Quantitative real-time PCR (RT-qPCR) and Western-blot (WB) assays were used to analyze gene and protein expression.
- SNHG6 and EZH2 expression levels were manipulated (silencing/overexpression).
Main Results:
- SNHG6 expression was elevated in EC cells and promoted proliferation, migration, and suppressed apoptosis.
- SNHG6 silencing significantly enhanced the sensitivity of EC cells (KYSE150, KYSE450) to 5-FU.
- SNHG6 promotes EC malignancy and 5-FU resistance by upregulating EZH2, which in turn modulates STAT3 and H3K27me3.
Conclusions:
- SNHG6 plays a crucial role in promoting EC progression and chemoresistance.
- Targeting SNHG6, potentially through modulating the EZH2/STAT3/H3K27me3 pathway, offers a promising therapeutic strategy to overcome 5-FU resistance in EC.
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