Tongbin Gao1, Yongjian Ji1. 1. Department of Urology, Weifang People's Hospital, Weifang, China.
Abstract
INTRODUCTION: Growing studies reveal that long noncoding RNA is involved in oncogenesis and progression. Previous studies have demonstrated that long intergenic noncoding RNA 00707 (LINC00707) stimulated tumor progress in numerous neoplasm types; however, the function of LINC00707 in bladder cancer (BC) was not yet clear. Our researches aimed to determine whether LINC00707 was dysregulated in BC and further study its biological functions. METHODS: LINC00707 levels in BC tissues and cells were measured using reverse transcription-PCR (RT-PCR), and the associations between the levels of LINC00707 and clinicopathological features and the months of survival were also examined. Then, Cell Counting Kit-8 assays, flow cytometry, colony formation assays, and Transwell assays were applied for the assessment of the impact of LINC00707 on the abilities of BC cells. The interaction between LINC00707 and miR-145 or cell division cycle associated 3 was determined by luciferase reporter system and RT-PCR. Protein expressions of Wnt/β-catenin signaling were examined using RT-PCR and Western blot. RESULTS: We found that LINC00707 expressions were notably upregulated in BC samples and cells. Higher expressions of LINC00707 were associated with T stage, grade, and shorter overall survival in BC patients. LINC00707 was also an independent prognostic factor for BC. In vitro assays confirmed that silencing LINC00707 expressions suppressed cell proliferation, colony formation, and metastasis. Mechanistic studies elucidated that LINC00707 was directly targeted to miR-145/CDCA3. Western blot assays revealed that Wnt/β-catenin signaling was inactivated by LINC00707 knockdown. CONCLUSION: Our work offers new insight into the function of LINC00707 in the tumorigenesis of BC.
INTRODUCTION: Growing studies reveal that long noncoding RNA is involved in oncogenesis and progression. Previous studies have demonstrated that long intergenic noncoding RNA 00707 (LINC00707) stimulated tumor progress in numerous neoplasm types; however, the function of LINC00707 in bladder cancer (BC) was not yet clear. Our researches aimed to determine whether LINC00707 was dysregulated in BC and further study its biological functions. METHODS: LINC00707 levels in BC tissues and cells were measured using reverse transcription-PCR (RT-PCR), and the associations between the levels of LINC00707 and clinicopathological features and the months of survival were also examined. Then, Cell Counting Kit-8 assays, flow cytometry, colony formation assays, and Transwell assays were applied for the assessment of the impact of LINC00707 on the abilities of BC cells. The interaction between LINC00707 and miR-145 or cell division cycle associated 3 was determined by luciferase reporter system and RT-PCR. Protein expressions of Wnt/β-catenin signaling were examined using RT-PCR and Western blot. RESULTS: We found that LINC00707 expressions were notably upregulated in BC samples and cells. Higher expressions of LINC00707 were associated with T stage, grade, and shorter overall survival in BC patients. LINC00707 was also an independent prognostic factor for BC. In vitro assays confirmed that silencing LINC00707 expressions suppressed cell proliferation, colony formation, and metastasis. Mechanistic studies elucidated that LINC00707 was directly targeted to miR-145/CDCA3. Western blot assays revealed that Wnt/β-catenin signaling was inactivated by LINC00707 knockdown. CONCLUSION: Our work offers new insight into the function of LINC00707 in the tumorigenesis of BC.