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Our results are consistent with previous findings in other
Our results are consistent with previous findings in other malignancies. Functional assays revealed that ectopic expression of UCA1 promoted cell proliferation and/or reduced cell apoptosis in non-small cell lung cancer [19], breast cancer [18], colorectal cancer [28], and renal cell carcinoma [23]. Knockdown of UCA1 impaired cell invasion or migration ability in breast cancer [29], esophageal squamous cell carcinoma [17], hepatocellular carcinoma[22], ovarian cancer [30], and melanoma [31]. UCA1 also decreased chemosensitivity in colorectal cancer[28], ovarian cancer [24], and neverless cancer [32]. Clinical investigation demonstrated that UCA1 overexpression was related to lymph node metastasis and advanced FIGO stage in ovarian cancer [24]. Increased UCA1 expression correlated with worse differentiation, large tumor size, deep local invasion, and advanced TNM stage in gastric cancer [33]. Further, high UCA1 expression was an unfavorable prognostic factor for overall survival of patients with esophageal squamous cell carcinoma [17], gastric cancer [33], colorectal cancer [21], hepatocellular carcinoma [22], and epithelial ovarian cancer [34]. Taken together, these research indicated the oncogenic functions of UCA1 in human cancers and suggested a potential application for UCA1 in molecular targeted therapy.
Conflicts of interest
Acknowledgement