Silencing NOB1 Can Affect Cell Proliferation and Apoptosis Via the C-Jun N-Terminal Kinase Pathway in Colorectal Cancer

Abstract

Objectives

To investigate the bio-functions and the molecular mechanisms of NIN1/proteasome 26S subunit non-ATPase 8 binding protein 1 homolog (NOB1) in colorectal cancer cells.

Methods

NOB1 expression was silenced using si-RNA in SW480 and LoVo cells. The transfection efficiency was measured by western blotting and RT-qPCR. Subsequently, the proliferation of SW480 and LoVo cells was determined using both MTT assay and colony-formation assay. Apoptosis and cell cycle analysis were determined using flow cytometry.

Results

Compared with the normal control (NC) and scramble cells, si-NOB1 could significantly attenuate the proliferation, colony-formation ability and cell percentage of S stage (p < 0.05). Additionally, at the phosphorylation level, si-NOB1 could notably increase the expression of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK) and p38.

Conclusions

Inhibition of NOB1 expression suppressed the proliferation, and promoted the apoptosis through regulation of the JNK signaling pathway.

Keywords:

• Colorectal cancer
• NIN1/proteasome 26S subunit non-ATPase 8 binding protein 1 homolog
• proliferation
• apoptosis
• c-Jun N-terminal kinase pathway

Acknowledgements

All authors would like to thank the support of Fu Dan University.

Disclosure statement

The authors declare that they have no competing interests.

Availability of data and materials

All data generated or analyzed during this study are included in this published article.

Authors' contributions

ZR and LY designed the research. JZL and ZQ performed the experiments. JL analyzed the data. LY wrote the paper.