Abstract:
:Colorectal cancer has become a disease with one of the highest incidence rates worldwide, and liver metastasis threatens the prognosis of colorectal cancer. MicroRNA (miR)‑200 and miR‑141 have been confirmed to be aberrantly expressed in colorectal cancer, however, whether miR‑200 and miR‑141 are involved in the progression of colorectal cancer, and their role in liver metastasis remain to be fully elucidated. The aim of the present study was to investigate the role of miR‑200 and miR‑141 in the progression and liver metastasis of colorectal cancer in patients. A total of 380 patients with colorectal cancer were enrolled, of which 142 were diagnosed with grade I/II disease and 238 were grade III/IV disease. Reverse transcription‑quantitative polymerase chain reaction analysis was performed to examine the serum levels of miR‑200 and miR‑141. In addition, transfection was performed in HCT116 and SW480 cells to establish overexpression models for miR‑200 and miR‑141. A TUNEL assay was performed to assess apoptosis and a Transwell experiment was performed to examine cell migration. Compared with the control group, the serum levels of miR‑200 and miR‑141 were significantly increased in the colorectal cancer group (P<0.05). Compared with the patients with colorectal cancer without liver metastasis, patients with liver metastasis had significantly higher serum levels of miR‑200 and miR‑141 (P<0.05). The overexpression of miR‑200 and miR‑141 inhibited apoptosis of the HC116 and SW480 cells, and enhanced cell migration. The upregulation of serum miR‑200 and miR‑141 were associated with liver metastasis in patients with colorectal cancer. Taken together, the overexpression of miR‑200 and miR‑141 exacerbated liver metastasis of colorectal cancer via inhibiting apoptosis and inducing migration.
journal_name
Mol Med Repjournal_title
Molecular medicine reportsauthors
Ding M,Zhang T,Li S,Zhang Y,Qiu Y,Zhang Bdoi
10.3892/mmr.2017.7538subject
Has Abstractpub_date
2017-11-01 00:00:00pages
7791-7795issue
5eissn
1791-2997issn
1791-3004journal_volume
16pub_type
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