ArticleOncology letters2020
POLR1B is upregulated and promotes cell proliferation in non-small cell lung cancer.
Article in Oncology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 20 citations in OpenAlex.
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Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to investigate the functions of RNA polymerase I subunit B (POLR1B) in lung cancer. Reverse transcription-quantitative PCR was used to measure the mRNA expression level of POLR1B in human lung cancer cell lines including A549, NCI-H1299, NCI-H1975 and NCI-H460. A lentivirus vector transfection system was used to knockdown POLR1B in A549 cells. The Celigo Cell Counting method, MTT and colony formation assays were used to investigate the proliferation of knocking-down POLR1B in A549 cells. Flow cytometry assay was used to investigate apoptosis rates. Co-expression analysis and microarray analysis were used to identify POLR1B targets in NSCLC. The Celigo Cell Counting method, MTT and colony formation assay revealed that the proliferation rates of lung cancer cells were significantly suppressed when POLR1B was silenced by lentivirus-mediated RNA interference. In addition, knocking-down the expression of POLR1B induced lung cancer cell apoptosis, visualized via flow cytometry. Bioinformatics revealed that POLR1B regulated multiple biological processes in NSCLC, including positive regulation of glucose import, and autophagosome assembly. The present study also identified several key targets of POLR1B, including ADRA1D, NR4A1, MYC, BOP1, DKC1, RRP12, IPO4, MTHFD2, CTPS1, GARS and NOC2L. The data from the present study suggest that POLR1B is an important modulator of lung cancer cell proliferation and indicate that POLR1B may be further selected as a potential anticancer therapeutic target for human lung cancer.
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