Yingbo Xue, Tingting Ni, Ying Jiang, Yong Li

Oncology Research, Vol.25, No.8, pp. 1305-1316, 2017, DOI:10.3727/096504017X14850182723737

Abstract Growth arrest-specific transcript 5 (GAS5) has been demonstrated to correlate with clinicopathological characteristics and serve as a tumor suppressor in non-small cell lung cancer (NSCLC). However, the underlying mechanism of the competing endogenous RNA (ceRNA) regulatory network involving GAS5 in NSCLC remains to be elucidated. In this study, qRT-PCR results showed that GAS5 was downregulated and miR-135b was upregulated in NSCLC tissues and cells. The expressions of GAS5 and miR-135b changed inversely in response to irradiation. Gain-of-function experiments revealed that GAS5 overexpression and miR-135b downregulation significantly suppressed tumorigenesis by repressing cell proliferation and invasion, and More >

Yongcheng Mei^*, Jinchun Si^†, Yun Wang^‡, Zhuangshi Huang^§, Haiwen Zhu^*, Shijun Feng^*, Xuezhi Wu^*, Liwen Wu^*

Oncology Research, Vol.25, No.6, pp. 1027-1037, 2017, DOI:10.3727/096504016X14822800040451

Abstract Previous studies reported that elevated expression of long noncoding RNA (lncRNA) GAS5 led to the arrest of non-small cell lung cancer (NSCLC) cell growth and a promotion of apoptosis both in vitro and in vivo. However, its underlying molecular mechanism in NSCLC is still unclear. In the present study, we noted that GAS5 was downregulated in NSCLC tissues and cells and was negatively correlated with miR-23a expression. Luciferase reporter assay and qRT-PCR analysis demonstrated that GAS5 directly interacted with miR-23a and reversely regulated its expression. miR-23a overexpression markedly promoted NSCLC cell proliferation and invasion, while More >

Wei Li, Weidong Zhao, Zhaohui Lu, Wen Zhang, Xuan Yang

Oncology Research, Vol.26, No.8, pp. 1285-1294, 2018, DOI:10.3727/096504018X15166193231711

Abstract Long noncoding RNA (lncRNA) growth arrest-specific transcript 5 (GAS5) has been revealed to be associated with the progression of various cancers. However, the biological roles of GAS5 in esophageal cancer (EC) remain unclear. We aimed to thoroughly explore the functions of GAS5 in EC. The results showed that GAS5 expression was increased in EC cells (ECA109, TE-1, TE-3, and EC9706) compared to SHEE cells. Knockdown of GAS5 decreased cell viability, migration, and invasion and induced apoptosis in EC9706 cells. Moreover, miR-301a appeared to be directly sponged by GAS5, and miR-301a suppression obviously alleviated the protumor More >