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Article

MicroRNA-103 promotes tumor growth and metastasis in colorectal cancer by directly targeting LATS2

  • Authors:
    • Yong‑Bin Zheng
    • Kuang Xiao
    • Gao‑Chun Xiao
    • Shi‑Lun Tong
    • Yu Ding
    • Qiu‑Shuang Wang
    • Sheng‑Bo Li
    • Zhi‑Nan Hao
  • View Affiliations / Copyright

    Affiliations: Department of Gastrointestinal Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China
  • Pages: 2194-2200
    |
    Published online on: July 5, 2016
       https://doi.org/10.3892/ol.2016.4814
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Abstract

Colorectal cancer (CRC) has become the third most common cancer worldwide and leads to a high mortality rate. Although colorectal cancer has been studied widely, the underlying molecular mechanism remains unclear. Increasing evidence shows that the abnormal expression of microRNAs (miRNAs) is involved in tumorigenesis. Previous studies have reported that miRNA-103 (miR-103) is dysregulated in CRC; however, the expression, function and mechanism of miR-103 in CRC are not well known. The present study showed that miR‑103 was overexpressed in the primary tumor tissues of patients with CRC and was significantly associated with a more aggressive phenotype of CRC in patients. Survival rate analysis demonstrated that CRC patients with high miR‑103 expression had a poorer overall survival compared with CRC patients with low miR‑103 expression. In CRC cell lines, miR‑103 inhibition significantly decreased the proliferation, invasion and migration of the cells in vitro. Furthermore, miR‑103 repressed large tumor suppressor kinase 2 (LATS2) expression by directly binding to the LATS2-3'-untranslated region, and an inverse correlation was identified between the expression of miR‑103 and LATS2 messenger RNA in primary CRC tissues. In addition, the restoration of LATS2 led to suppressed proliferation, invasion and migration of CRC cells. In vivo, miR‑103 promotes tumor growth in nude mice. In summary, miR‑103 performs a critical role in the promotion of the invasive and metastatic capacities of CRC, possibly by directly targeting LATS2. This miRNA may be involved in the development and progression of CRC.
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Copy and paste a formatted citation
Spandidos Publications style
Zheng YB, Xiao K, Xiao GC, Tong SL, Ding Y, Wang QS, Li SB and Hao ZN: MicroRNA-103 promotes tumor growth and metastasis in colorectal cancer by directly targeting LATS2. Oncol Lett 12: 2194-2200, 2016.
APA
Zheng, Y., Xiao, K., Xiao, G., Tong, S., Ding, Y., Wang, Q. ... Hao, Z. (2016). MicroRNA-103 promotes tumor growth and metastasis in colorectal cancer by directly targeting LATS2. Oncology Letters, 12, 2194-2200. https://doi.org/10.3892/ol.2016.4814
MLA
Zheng, Y., Xiao, K., Xiao, G., Tong, S., Ding, Y., Wang, Q., Li, S., Hao, Z."MicroRNA-103 promotes tumor growth and metastasis in colorectal cancer by directly targeting LATS2". Oncology Letters 12.3 (2016): 2194-2200.
Chicago
Zheng, Y., Xiao, K., Xiao, G., Tong, S., Ding, Y., Wang, Q., Li, S., Hao, Z."MicroRNA-103 promotes tumor growth and metastasis in colorectal cancer by directly targeting LATS2". Oncology Letters 12, no. 3 (2016): 2194-2200. https://doi.org/10.3892/ol.2016.4814
Copy and paste a formatted citation
x
Spandidos Publications style
Zheng YB, Xiao K, Xiao GC, Tong SL, Ding Y, Wang QS, Li SB and Hao ZN: MicroRNA-103 promotes tumor growth and metastasis in colorectal cancer by directly targeting LATS2. Oncol Lett 12: 2194-2200, 2016.
APA
Zheng, Y., Xiao, K., Xiao, G., Tong, S., Ding, Y., Wang, Q. ... Hao, Z. (2016). MicroRNA-103 promotes tumor growth and metastasis in colorectal cancer by directly targeting LATS2. Oncology Letters, 12, 2194-2200. https://doi.org/10.3892/ol.2016.4814
MLA
Zheng, Y., Xiao, K., Xiao, G., Tong, S., Ding, Y., Wang, Q., Li, S., Hao, Z."MicroRNA-103 promotes tumor growth and metastasis in colorectal cancer by directly targeting LATS2". Oncology Letters 12.3 (2016): 2194-2200.
Chicago
Zheng, Y., Xiao, K., Xiao, G., Tong, S., Ding, Y., Wang, Q., Li, S., Hao, Z."MicroRNA-103 promotes tumor growth and metastasis in colorectal cancer by directly targeting LATS2". Oncology Letters 12, no. 3 (2016): 2194-2200. https://doi.org/10.3892/ol.2016.4814
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