4.6 Article

LINC00857 knockdown inhibits cell proliferation and induces apoptosis via involving STAT3 and MET oncogenic proteins in esophageal adenocarcinoma

期刊

AGING-US
卷 11, 期 9, 页码 2812-2821

出版社

IMPACT JOURNALS LLC
DOI: 10.18632/aging.101953

关键词

LINC00857; esophageal adenocarcinoma; proliferation; apoptosis

资金

  1. National Natural Science Foundation of China (NSFC) [81702270, 81871883, 81803564]
  2. Affiliated Hospital of Guangdong Medical University Doctoral Foundation [2018052638]
  3. Guangxi Natural Science Foundation [2015GXNSF BA139117]
  4. China Postdoctoral Science Foundation [2018M633619XB]
  5. Medical Discipline Reserve Talents of Yunnan Province [H-2017037]

向作者/读者索取更多资源

Esophageal adenocarcinoma (EAC) is one of the leading causes of cancer-related death worldwide, and the molecular biology of this cancer remains poorly understood. Recent evidence indicates that long non-coding RNAs are dysregulated in a variety of cancers including EAC. In this study, siRNA mediated gene knockdown, Western blot, RT-PCR, as well as oncogenic function assay were performed. We found that the cell proliferation, colony formation, invasion and migration were decreased after LINC00857 knockdown in EAC cell lines. We also found that knockdown LINC00857 could induce apoptosis. Mechanistically, we found that the MET, STAT3, c-Myc and p-CREB proteins were decreased after LINC00857 knockdown. Our study suggests that LINC00857 may play an important oncogenic role in EAC via STAT3 and MET signaling.

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