Abstract

Long non-coding RNAs (lncRNAs) are a family of non-protein-coding RNAs that might affect Lung adenocarcinoma (LAD) chemo-resistance and most of them could be used as biomarkers and therapy targets. However, the potential function of lncRNA ANRIL contributed paclitaxel chemo-resistance in LAD is still unknown. This study aimed to observe the expression of ANRIL in LAD, evaluate its biological role in the resistance of LAD cells to paclitaxel and explore the apoptosis role in the ANRIL associated mechanism. Our results showed that ANRIL functioning as a potential oncogene was up-regulated in LAD, and promoted the acquisition of chemo-resistance in paclitaxel partly through the mitochondrial pathway by modulating the expression of apoptosis-related protein cleaved-PARP and Bcl-2. These findings might improve LAD patients' paclitaxel treatment and made ANRIL to be a new target for paclitaxel-based chemotherapy in LAD.

Highlights

  • Lung cancer, with the first morbidity and the second death rate, is one of the common cancers occurred in both males and females in the world

  • Long non-coding RNAs are a family of non-protein-coding RNAs, which have been identified as oncogenes or tumor suppressors that are involved in a variety of diseases, including cancer [5,6,7]

  • The results revealed the expression of ANRIL was associated with the TNM stage and differentiation grade no matter patients were sensitive or insensitive to the paclitaxel associated chemotherapy

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Summary

Introduction

With the first morbidity and the second death rate, is one of the common cancers occurred in both males and females in the world. Long non-coding RNAs (lncRNAs) are a family of non-protein-coding RNAs, which have been identified as oncogenes or tumor suppressors that are involved in a variety of diseases, including cancer [5,6,7]. ANRIL, known as CDKN2B antisense RNA1, was originally identified in the familial melanoma patients. It is located within the CDKN2B-CDKN2A gene cluster at chromosome 9p21 [8, 9]. Since its identification, accumulating studies have showed that ANRIL may function as an oncogene and act as key players in many cancers, in the cardiovascular disease [9,10,11]. The expression of ANRIL and its functional mechanisms in paclitaxel- resistant LAD are still ambiguous

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