Abstract
BackgroundLong non-coding RNA (lncRNA) was a vital factor in the progression and initiation of human cancers. This study found a new lncRNA, FGD5-AS1, which can inhibit EMT process, proliferation, and metastasis in vitro and in vivo.MethodsqRT-PCR was employed to test the expression of lncFGD5-AS1 in 30 gastric cancer patients’ cancer tissue and para-cancer tissue. Overexpressed lncFGD5-AS1 cells shown sharply decrease of proliferation, migration, and epithelial-mesenchymal transition (EMT). miR-196a-5p/SMAD6 was confirmed as downstream molecular mechanism of lncFGD5-AS1 by expression correlation analysis and mechanism experiments. In vivo study illustrated overexpression of lncFGD5-AS1 suppression tumor growth.ResultsLncFGD5-AS1 served as a ceRNA of miR-196a-5p to release its inhibition on SMAD6, a conventional inhibitor on the BMP pathway. Comparing with normal gastric cancer cells, FGD5-AS1 overexpressed group had fewer migration cells, lower cell viability, and lower EMT transformation rate. Meanwhile, xenografts nude mice injecting with overexpressed-FGD5-AS1 cells also shown smaller tumor weight and volume.ConclusionIn conclusion, this research supported the first evidence that FGD5-AS1 suppressed proliferation and metastasis in gastric cancer by regulating miR-196a-5p/SMAD6/BMP axis and suggested a potential therapeutic candidate for gastric cancer.
Highlights
IntroductionLong non-coding RNA (lncRNA) was a vital factor in the progression and initiation of human cancers
Long non-coding RNA was a vital factor in the progression and initiation of human cancers
Lower level of Long non-coding RNA (lncRNA) FGD5-AS1 indicated a worse prognosis To investigate the potential relationship between FGD5AS1 and the cancer process, we compared FGD5-AS1 levels in 30 patients’ tumor tissue and para-cancer normal tissue
Summary
Long non-coding RNA (lncRNA) was a vital factor in the progression and initiation of human cancers. According to the clinical research carried out in 2013, gastric cancer is the third most common and the third lethal tumor [1]. On the complex development of tumor initiation to metastasis, cancer cells need to adapt to permanently changing and often hostile environmental conditions. To survive in these conditions, tumor cells lose their epithelial feature and change to mesenchymal traits. With these changes, tumor cells show high migration, invasion, and survival features. Tumor cells show high migration, invasion, and survival features These features are the core of tumor associated epithelial–mesenchymal transition (EMT). EMT has became a highlight point in cancer treatment research
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