Abstract | OBJECTIVES: 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.
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Authors | Zhong Ren, Liqing Yao, Jingzheng Liu, Zhipeng Qi, Jian Li |
Journal | Journal of investigative surgery : the official journal of the Academy of Surgical Research
(J Invest Surg)
Vol. 34
Issue 8
Pg. 819-825
(Aug 2021)
ISSN: 1521-0553 [Electronic] United States |
PMID | 31906747
(Publication Type: Journal Article)
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Chemical References |
- NOB1 protein, human
- Nuclear Proteins
- RNA-Binding Proteins
- JNK Mitogen-Activated Protein Kinases
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Topics |
- Apoptosis
- Cell Line, Tumor
- Cell Proliferation
- Colorectal Neoplasms
(genetics)
- Humans
- JNK Mitogen-Activated Protein Kinases
- Nuclear Proteins
(metabolism)
- RNA-Binding Proteins
(genetics)
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