miR‐106a is frequently upregulated in gastric cancer and inhibits the extrinsic apoptotic pathway by targeting FAS

Abstract

Emerging evidence has shown the association of aberrantly expressed miR-106a with cancer development, however, little is known about its potential role in gastric carcinogenesis. In our present study, obviously overexpressed miR-106a was found in gastric cancer tissues compared with their nontumor counterparts. Suppression of miR-106a significantly inhibited gastric cancer cell proliferation and triggered apoptosis. Bioinformatic analysis combining with validation experiments identified FAS as a direct target of miR-106a. Rescue experiments and examination of caspase-8, PARP and caspase-3 further approved that miR-106a could inhibit gastric cancer cell apoptosis through interfering with FAS-mediated apoptotic pathway. Moreover, a significant inverse correlation was found between miR-106a and FAS expression not only in gastric cancer cell lines but also in gastric cancer specimens. Taken together, these findings suggest that ectopicly overexpressed miR-106a may play an oncogenic role in gastric carcinogenesis and impair extrinsic apoptotic pathway through targeting FAS.

MicroRNA-106a promotes cell migration and invasion by targeting tissue inhibitor of matrix metalloproteinase 2 in cervical cancer

“…These data strongly support our present data in regards to CC. Moreover, miR-106a was frequently upregulated in gastric cancer and inhibited the extrinsic apoptotic pathway by targeting FAS (13). In addition, miR-106a targeted autophagy and enhanced sensitivity of lung cancer cells to Src inhibitors (29).…”

“…Accumulating studies have confirmed that aberrant expression of miRNAs is involved in various types of cancer, including CC, and participate in diverse biological processes such as cell growth, invasion, differentiation and metastasis (8)(9)(10)(11)(12). Recently, miR-106a, which is derived from the precursor miR-106a-363 on chromosome Xq26.2, was revealed to play a critical role in the progression of cancers (13)(14)(15)(16)(17). A previous study revealed that miR-106a functions as a regulator of cell invasion, proliferation and drug sensitivity (18).…”

MicroRNA-106a regulates phosphatase and tensin homologue expression and promotes the proliferation and invasion of ovarian cancer cells

“…In the present study, we identified the deregulation of miR-106a in ovarian cancer. miR-106a is widely expressed in diverse human tumors, including gastric, non-small cell lung, pancreatic, colorectal and ovarian cancer (6,8,9,(43)(44)(45)(46)(47)(48)(49)(50)(51)(52)(53). Previous studies showed that miR-106a acts as a tumor suppressor or an oncogene in different cancers, depending on the different cellular context.…”

“…Previous studies showed that miR-106a acts as a tumor suppressor or an oncogene in different cancers, depending on the different cellular context. In gastric cancer, expression of miR-106a was increased, and downregulation of the expression of miR-106a inhibited gastric cancer cell proliferation and caused apoptosis by targeting FAS (52). In non-small cell lung cancers, miR-106a inhibited the growth and metastasis of NSCLC cells by decreasing phosphatase and tensin homolog (PTEN) expression (9).…”

miR-106a confers cisplatin resistance by regulating PTEN/Akt pathway in gastric cancer cells

“…Wang et al [10] have found that miR-106a is among the most highly expressed miRNAs in human gastric cancer cell lines and in primary gastric tumors. It also has been reported that the upregulation of miR-106a promotes survival of esophageal adenocarcinoma cells and confers resistance to DDP [11].…”