Abstract
Dysregulation of microRNA expression is involved in several pathological activities associated with gastric cancer progression and chemo-resistance. However, the role and molecular mechanisms of miR-363 in the progression and chemo-resistance of gastric cancer remain enigmatic. In this study, we validated that miR-363 expression was higher in gastric cancer tissues than in adjacent normal tissues. Multivariate analysis identifies high levels of miR-363 expression as an independent predictor for postoperative recurrence and lower overall survival. Increased miR-363 expression promotes gastric cancer cell proliferation and chemo-resistance through directly targeting the tumor suppressor F-box and WD repeat domain-containing 7 (FBW7). Clinically, our data reveal that overexpression of miR-363 correlates with the poor survival outcomes in patients with gastric cancer, and docetaxel + cisplatin + 5-FU (DCF) regimen response is impaired in patients with miR-363 overexpression. These data suggest that miR-363 may be a potential therapeutic target for gastric cancer and serve as a biomarker for predicting response to DCF regimen treatment.
Highlights
Gastric cancer is the fourth most common cancer and second leading cause of cancer-related deaths worldwide [1]
As the poor prognosis in gastric cancer patients is mainly due to late diagnosis and bad chemotherapy response, it is urgently needed to identify predictive markers of therapeutic response
Evidences suggests the roles of miRNAs, including influence of therapeutic induced cell apoptosis, regulation of multiple drug resistance (MDR)-related proteins expression, and induction of cancer cells converting to tumor stem-like cells (TSC) in several cancers [27]
Summary
Gastric cancer is the fourth most common cancer and second leading cause of cancer-related deaths worldwide [1]. Patients with advanced gastric cancer have a poor prognosis and the 5-year overall survival rate remains low at approximately 25% [1,2,3]. These dismal outcomes result from its high recurrence following curative stomach resection and its notorious resistance to systemic chemotherapy [4, 5]. For patients with advanced gastric cancer, the response rate to neoadjuvant chemotherapy is more than 50% and most patients develop chemotherapy resistance [7]. It is urgently needed to identify and develop new treatment strategies regarding gastric cancer molecular mechanisms involved in chemotherapy resistance
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