Abstract
Despite the growing number of studies exhibiting an association of diabetes mellitus (DM) and lung cancer progression, the concrete mechanism of DM aggravating lung cancer has not been elucidated. The present study was to investigate whether and how high glucose (HG) contributes to the proliferation and migration of non-small-cell lung cancer (NSCLC) cells in vitro. In the present study, we confirmed that HG promoted the proliferation and migration of NSCLC cells, and also induced an anti-apoptotic effect on NSCLC cells. Moreover, HG inhibited the expression of growth arrest-specific 5 (GAS5) in NSCLC cells but elevated the protein level of tribbles homolog 3 (TRIB3). GAS5 overexpression promoted the degradation of TRIB3 protein by ubiquitination and inhibited the HG-induced proliferation, anti-apoptosis, and migration of NSCLC cells. Importantly, TRIB3 overexpression reversed the effects of GAS5 on the HG-treated NSCLC cells. Taken together, down-regulated GAS5 by HG significantly enhanced the proliferation, anti-apoptosis, and migration in NSCLC cells through TRIB3, thus promoting the carcinogenesis of NSCLC.
Highlights
Lung cancer is one of the most common malignant tumors with the highest morbidity and mortality that seriously threatens human health and life [1]
Further studies revealed that transfection of pcDNA-growth arrest-specific 5 (GAS5) in Non-small-cell lung cancer (NSCLC) cells disinhibited the GAS5 depression derived from High gluose (HG) treatment and GAS5 expression was significantly increased (Figure 1D)
HG inhibited the expression of Long non-coding RNA (lncRNA) GAS5 in NSCLC cells but elevated the protein level of tribbles homolog 3 (TRIB3)
Summary
Lung cancer is one of the most common malignant tumors with the highest morbidity and mortality that seriously threatens human health and life [1]. As the high-risk factor for malignant tumors, the mortality rate of tumor patients with diabetes mellitus (DM) was significantly higher than those without DM. Some mechanisms have been hypothesized to explore how an excess level of glucose affected the occurrence and development of tumors, such as breast, colorectal, pancreatic, and lung cancer [8,9,10]. Despite the growing number of studies exhibited an association c 2018 The Author(s).
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