Aldolase A promotes proliferation and G1 /S transition via the EGFR/MAPK pathway in non-small cell lung cancer

Cancer Communications
Hailu FuShujuan Shao

Abstract

Our previous study demonstrated that aldolase A (ALDOA) is overexpressed in clinical human lung squamous cell carcinoma and that ALDOA promotes epithelial-mesenchymal transition and tumorigenesis. The present study aimed to explore the function of ALDOA in the modulation of non-small cell lung cancer (NSCLC) proliferation and cell cycle progression and the potential mechanism. ALDOA was knocked down by short hairpin RNA in H520 and H1299 cells. ALDOA was overexpressed with vectors carrying the full-length ALDOA sequence in H1299 and H157 cells. The proliferation capacities were assessed with immunohistochemical staining, Cell Counting Kit-8 and colony formation assays. The cell cycle distribution was examined by flow cytometry, and molecular alterations were determined by western blotting. Cell synchronization was induced with nocodazole. The stability of cyclin D1 mRNA was tested. The pyruvate kinase M2 and ALDOA protein distributions were examined. Aerobic glycolysis was evaluated with Cell Titer-Glo assay, glucose colorimetric assay and lactate colorimetric assay. ALDOA knockdown inhibited the proliferation and G1/S transition in H520 cells. Conversely, ALDOA overexpression promoted the proliferation and G1/S transition in H...Continue Reading

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Apr 5, 2020·Molecules : a Journal of Synthetic Chemistry and Natural Product Chemistry·Chien-Ming LiuYi-Hsien Hsieh
Jan 1, 2021·Cancer Management and Research·Ying ChuJie Ma
May 15, 2021·Frontiers in Cell and Developmental Biology·Rui MaXilan Yu

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Methods Mentioned

BETA
xenograft
transfection
xenografts
flow cytometry
Assay
PCR
nuclear translocation

Software Mentioned

ALDOA
SPSS

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