• 2018-07
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  • 2018-11
  • 2019-04
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  • 2019-06
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  • 2020-01
  • Our results are consistent with previous findings in other m


    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 phospholipase c inhibitor 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 phospholipase c inhibitor 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