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Knockdown of PAF1 reduces cervical cancer cell proliferation, migration and invasion via retarding FLOT2-mediated MEK/ERK1/2 pathway.

ABSTRACT: Cervical cancer (CC) is a very usual reproductive malignant tumor in women. RNA polymerase II-associated factor 1 (PAF1) and flotillin-2 (FLOT2) both have been discovered to key participators in cancers' progression. However, the effects of PAF1/FLOT2 axis on CC development have not been probed. In this study, PAF1 and FLOT2 exhibited higher expression, and silencing of PAF1 down-regulated FLOT2 expression in CC. In addition, the regulatory effects of PAF1 suppression on CC progression were reversed after FLOT2 overexpression. Next, inhibition of PAF1 slowed the tumor growth in vivo through modulating FLOT2. Besides, down-regulation of PAF1 reduced FLOT2 expression to retard the MEK/ERK1/2 pathway. In conclusion, knockdown of PAF1 suppressed CC progression via retarding FLOT2-mediated MEK/ERK1/2 pathway. Our findings illustrated that the PAF1/FLOT2 axis may be useful bio-targets for CC treatment.

SUBMITTER: Tang B

PROVIDER: S-EPMC10538450 | biostudies-literature | 2023 Dec

REPOSITORIES: biostudies-literature

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Knockdown of PAF1 reduces cervical cancer cell proliferation, migration and invasion via retarding FLOT2-mediated MEK/ERK1/2 pathway.

Tang Bin B Dou Shulan S

Cell adhesion & migration 20230927 1

Cervical cancer (CC) is a very usual reproductive malignant tumor in women. RNA polymerase II-associated factor 1 (PAF1) and flotillin-2 (FLOT2) both have been discovered to key participators in cancers' progression. However, the effects of PAF1/FLOT2 axis on CC development have not been probed. In this study, PAF1 and FLOT2 exhibited higher expression, and silencing of PAF1 down-regulated FLOT2 expression in CC. In addition, the regulatory effects of PAF1 suppression on CC progression were reve ...[more]

PMID: 37754347

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Project description:BackgroundNADH: ubiquinone oxidoreductase subunit C1(NDUFC1) encodes a subunit of the Complex I, which may support the structural stability of Complex I and assist in its biogenesis. The expression and functional roles of NDUFC1 in hepatocellular carcinoma (HCC) remain unknown.ResultWe knocked down the expression of NDUFC1 in HCC cell lines to explore the effects of NDUFC1 downregulation on HCC in vitro. MTT assay determined that downregulation of NDUFC1 significantly inhibited cell proliferation. Flow cytometry with (propidium iodide) PI staining indicated silencing of NDUFC1 arrested cell cycle of BEL-7404 cells at G2 phase and SK-HEP-1 cells at S/G2 phase. Annexin V-PI double staining and flow cytometric analysis showed that the downregulation of NDUFC1 significantly increased the population of apoptotic cells. Wound-healing assay and transwell assay indicated that the downregulation of NDUFC1 suppressed the migration and invasion of HCC cells. According to the detection of complex1 activity, we found that the activity of NDUFC1 silenced group decreased, whereas the content of ROS increased. Furthermore, combined with bioinformatics analysis of senescence-related genes, we found that the silence of NDUFC1 in HCC could induce senescence and inhibit autophagy. In addition, NDUFC1 could correlate positively with cancer-related pathways, among which the p53 pathways and the PI3K/Akt/mTOR pathways. Finally, NDUFC1 is high expression in HCC specimens. High NDUFC1 expression was associated with poor prognosis and was an independent risk factor for reduced overall survival (OS).ConclusionsOur study indicated, for the first time, that NDUFC1 is an independent risk factor for the poor prognosis of HCC patients. NDUFC1 may promote tumor progression by inhibiting mitochondrial Complex I and up-regulating ROS through multiple cancer-related and senescence-related pathways of HCC, including p53 pathways and PI3K/Akt/mTOR pathways. We suppose that NDUFC1 might be a potential target for the mitochondrial metabolism therapy of HCC.

Dataset Information

Knockdown of PAF1 reduces cervical cancer cell proliferation, migration and invasion via retarding FLOT2-mediated MEK/ERK1/2 pathway.

Publications

Knockdown of PAF1 reduces cervical cancer cell proliferation, migration and invasion via retarding FLOT2-mediated MEK/ERK1/2 pathway.

Similar Datasets

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