4.6 Article

Elevated LOXL2 expression by LINC01347/miR-328-5p axis contributes to 5-FU chemotherapy resistance of colorectal cancer

期刊

AMERICAN JOURNAL OF CANCER RESEARCH
卷 11, 期 4, 页码 1572-1585

出版社

E-CENTURY PUBLISHING CORP

关键词

Colorectal cancer; 5-FU; chemotherapy resistance; LINC01347; LOXL2; miR-328-5p

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资金

  1. National Natural Science Foundation of China [81972793, 81803400, 81602730, 81502283]
  2. Shinan District Science and Technology Plan, Qingdao [2016-3-020-YY, 20184026YY]
  3. Shandong province Medical Health Science and Technology Project [2018WS447]
  4. Qingdao Science and Technology Program for Benefiting People Special Project 2019 [196125nsh]
  5. Qingdao Outstanding Health Professional Development Fund

向作者/读者索取更多资源

Elevated expression of LINC01347 is associated with disease progression and poor prognosis in colorectal cancer (CRC) patients undergoing chemotherapy. LINC01347 may play a role in promoting cell proliferation and resistance to 5-FU in CRC cells, potentially through regulation of LOXL2 via miR-328-5p. Identification of LINC01347 as a prognostic biomarker and therapeutic target highlights its potential in overcoming chemotherapy resistance in CRC.
Chemotherapy resistance after curative surgery is a major contributor to the mortality of colorectal cancer (CRC). Detailed mechanism studies of specific molecular alterations are critical to improving the available therapies for long-term disease administration. We explored the functional role of LINC01347 in chemotherapy resistance of CRC. Elevated LINC01347 expression was correlated with CRC disease progression during chemotherapy treatment. However, the functional role of LINC01347 and mechanism remained undefined. In this study, we demonstrated that elevated LINC01347 expression was correlated with late clinical stage and poor prognosis in CRC tumor tissues with TCGA data. Exogenous LINC01347 expression promoted cell proliferation and 5-FU resistance of CRC cells, while LINC01347 knockdown attenuated cell growth and 5-FU resistance in vitro and in vivo. Molecular analysis indicated that LINC01347 participated in the transcriptional regulation of LOXL2 by sponging miR-328-5p. LOXL2 knockdown impaired the LINC01347 overexpression induced 5-FU resistance in CRC cells. The clinical analysis supported miR-328-5p/LOXL2 as a candidate biomarker for chemotherapy resistance of CRC patients. Our study provided a molecular basis for the development of 5-FU based chemotherapy resistance in CRC by LINC01347/miR-328/LOXL2 axis. We identified LINC01347 as a prognostic biomarker and potential therapeutic target against 5-FU based chemotherapy resistance of CRC.

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