Open Access

Silencing Lin28 promotes apoptosis in colorectal cancer cells by upregulating let‑7c targeting of antiapoptotic BCL2L1

  • Authors:
    • Haogang Zhang
    • Yaguang Zong
    • Gongcai Qiu
    • Ruichun Jia
    • Xunzheng Xu
    • Fujing Wang
    • Dequan Wu
  • View Affiliations

  • Published online on: January 25, 2018     https://doi.org/10.3892/mmr.2018.8483
  • Pages: 5143-5149
  • Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Colorectal cancer (CRC) remains a primary contributor to cancer‑associated mortality. The Lin28/let‑7 axis has previously been verified to participate in numerous pathophysiological processes involved in CRC. However, the potential roles and underlying mechanisms of this axis in apoptosis during CRC remain to be fully elucidated. The present study aimed to evaluate the role and reveal the molecular mechanisms of the Lin28/let‑7 axis in the apoptosis of CRC cells. An MTT assay was conducted to assess the cell viability of HCT116 and HT29 CRC cells, and caspase‑3 activity was analyzed to measure the apoptosis of CRC cells. Western blotting and reverse transcription‑quantitative polymerase chain reaction were performed to examine the expression of Lin28, B‑cell lymphoma 2 (Bcl‑2), Bcl‑2‑associated X protein, Bcl‑2‑like 1 (BCL2L1) and let‑7c. The present study demonstrated that Lin28 was upregulated whereas let‑7c was downregulated in CRC tissues and cell lines compared with normal tissues and NCM460 normal colon epithelial cells, respectively. Forced overexpression of let‑7c promoted apoptosis in CRC cells, which was at least partially mediated via the targeting of BCL2L1. Furthermore, knockdown of Lin28 decreased viability and promoted apoptosis in CRC cells, whereas this effect was attenuated by let‑7c inhibition. The findings of the present study suggest the involvement of the Lin28/let‑7c axis in apoptosis during CRC, and indicate the potential role of this pathway as a novel therapeutic target in CRC.
View Figures
View References

Related Articles

Journal Cover

April-2018
Volume 17 Issue 4

Print ISSN: 1791-2997
Online ISSN:1791-3004

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Zhang H, Zong Y, Qiu G, Jia R, Xu X, Wang F and Wu D: Silencing Lin28 promotes apoptosis in colorectal cancer cells by upregulating let‑7c targeting of antiapoptotic BCL2L1. Mol Med Rep 17: 5143-5149, 2018.
APA
Zhang, H., Zong, Y., Qiu, G., Jia, R., Xu, X., Wang, F., & Wu, D. (2018). Silencing Lin28 promotes apoptosis in colorectal cancer cells by upregulating let‑7c targeting of antiapoptotic BCL2L1. Molecular Medicine Reports, 17, 5143-5149. https://doi.org/10.3892/mmr.2018.8483
MLA
Zhang, H., Zong, Y., Qiu, G., Jia, R., Xu, X., Wang, F., Wu, D."Silencing Lin28 promotes apoptosis in colorectal cancer cells by upregulating let‑7c targeting of antiapoptotic BCL2L1". Molecular Medicine Reports 17.4 (2018): 5143-5149.
Chicago
Zhang, H., Zong, Y., Qiu, G., Jia, R., Xu, X., Wang, F., Wu, D."Silencing Lin28 promotes apoptosis in colorectal cancer cells by upregulating let‑7c targeting of antiapoptotic BCL2L1". Molecular Medicine Reports 17, no. 4 (2018): 5143-5149. https://doi.org/10.3892/mmr.2018.8483