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Chinese Journal of Geriatrics Research(Electronic Edition) ›› 2020, Vol. 07 ›› Issue (04): 21-26. doi: 10.3877/cma.j.issn.2095-8757.2020.04.004

Special Issue:

• Original Article • Previous Articles     Next Articles

The role of kinesin family member 18A in the progression of lung adenocarcinoma

Ju Yang1, Futao Chen1,(), Fukuan Zhong1, Lifeng Cao1, Jiang Zhu1, Yingying Liao1   

  1. 1. Department of Respiratory, the Second Hospital of Lianyungang, Lianyungang 222000, China
  • Received:2020-04-30 Online:2020-11-28 Published:2021-03-19
  • Contact: Futao Chen

Abstract:

Objective

To investigate the expression of kinesin family member 18A (KIF18A) in lung adenocarcinoma and its role in the progression of lung adenocarcinoma.

Methods

102 lung adenocarcinoma patients admitted to the Second Hospital of Lianyungang from April 2014 to May 2018 were selected, and lung adenocarcinoma tissues and adjacent tissues were collected. The expression of KIF18A in lung adenocarcinoma and adjacent normal tissues was detected by immunohistochemistry. The effect of KIF18A on the proliferation, migration and invasion of lung adenocarcinoma cells was observed by cell experiment in vitro, and the effect of KIF18A on tumor growth and metastasis in mice was observed.

Results

Immunohistochemical analysis showed that KIF18A was mainly expressed in the cytoplasm of lung adenocarcinoma cells, while the expression level of KIF18A was significantly lower in adjacent tissues. Quantitative PCR showed that the expression of KIF18A in A549 and H1975 cells was effectively inhibited after transfection of KIF18A shRNA plasmid. Western blot analysis showed that the expression level of KIF18A in A549 and H1975 cells transfected with KIF18A shRNA plasmid decreased significantly. Colony determination showed that consumption of KIF18A significantly reduced the number of colonies. MTT detection showed that the absorbance value of two types of lung adenocarcinoma cells at 570 nm was significantly decreased. Wound healing test showed that KIF18A depletion significantly inhibited the wound healing of A549 and H1975 cells. Transwell experiment showed that the depletion of KIF18A significantly blocked the invasion of A549 and H1975 cells, and the number of cells decreased significantly. Animal experiment showed that the tumor volume of KIF18A knockout mice was significantly smaller than that of the control group, and the expression level of KIF18A was also significantly reduced; after 8 weeks of tumor metastasis, the incidence of lung metastasis of A549 cells was significantly lower than that of the control group.

Conclusion

KIF18A is involved in the progression and metastasis of lung adenocarcinoma, which will provide a new possibility for targeted therapy of lung adenocarcinoma.

Key words: Lung adenocarcinoma, Kinesin Family member 18A, Proliferation, Migration, Invasion, Therapeutic target

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