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Downregulation of TMOD1 promotes cell motility and cell proliferation in cervical cancer cells.

ABSTRACT: Tropomodulin-1 (TMOD1) is a key regulator of actin dynamics, which caps the pointed end of actin filaments. TMOD1 has been reported to be involved in several cellular processes, including neurite outgrowth, spine formation and cell migration. Increasing evidence demonstrates that TMOD1 is implicated in several aspects of cancer development. The present study aimed to investigate the role of TMOD1 in cervical cancer. HeLa and CaSki cell lines, derived from human cervical cancer, were used to evaluate the function of TMOD1. Cell motility was measured via a wound-healing assay, with the TMOD1 short hairpin (sh)RNAs transfected cells. Subsequently, cell proliferation was assessed using low serum cell culture condition, while cell cycle distribution was analyzed via flow cytometry. The results demonstrated that downregulated TMOD1 promoted cell motility and proliferation, which is attributed to promotion of G1/S phase transition in HeLa and CaSki cells. Furthermore, it was indicated that co-expression of shRNA resistant TMOD1 rescued these phenomena. The clinical data demonstrated that high TMOD1 expression is associated with good pathological status in patients with cervical cancer. Overall, the results of the present study indicated that TMOD1 may act as a tumor suppressor in cervical cancer, whereby its downregulated expression was demonstrated to have direct effects on cell motility and cell proliferation. These results provide new evidence for the prognostic prediction of cervical cancer, which may serve as a promising therapeutic strategy for patients with cervical cancer.

SUBMITTER: Lu F

PROVIDER: S-EPMC7068698 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature

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Downregulation of TMOD1 promotes cell motility and cell proliferation in cervical cancer cells.

Lu Fangjin F Cui Dandan D Mu Bin B Zhao Lu L Mu Ping P

Oncology letters 20200219 4

Tropomodulin-1 (TMOD1) is a key regulator of actin dynamics, which caps the pointed end of actin filaments. TMOD1 has been reported to be involved in several cellular processes, including neurite outgrowth, spine formation and cell migration. Increasing evidence demonstrates that TMOD1 is implicated in several aspects of cancer development. The present study aimed to investigate the role of TMOD1 in cervical cancer. HeLa and CaSki cell lines, derived from human cervical cancer, were used to eval ...[more]

PMID: 32218869

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Project description:Background The deubiquitinating (DUB) enzyme ubiquitin-specific protease 18 (USP18), also known as UBP43, is an ubiquitin-specific protease linked to several human malignancies. However, USP18’s underlying function in human cervical cancer remains unclear. In the current study, we aimed to analyse the role of USP18 and its signalling pathways in cervical cancer. Methods Quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemical staining were performed to analyse USP18 levels in cervical cancer and matched to adjacent normal tissues. Moreover, RNA interference (RNAi) and lentiviral-mediated vector transfections were performed to silence and overexpress USP18, respectively, in cervical cancer cells. Further, Cell Counting Kit-8 (CCK-8) and Annexin V/PI staining assays were used to assess its biological function in cell proliferation and apoptosis, respectively. A xenograft model was used to examine USP18’s function in vivo. Results The present findings demonstrated that USP18 was overexpressed in cervical cancer specimens and cell lines. Silencing USP18 in SiHa and Caski cervical cancer cell lines inhibited cell proliferation, induced apoptosis, and promoted cleaved caspase-3 expression. In contrast, USP18 overexpression showed the opposite effects in human HcerEpic cells. A Gene Set Enrichment Analysis revealed that USP18 was enriched in the PI3K/AKT signalling pathway in cervical cancer. Hence, the PI3K/AKT inhibitor LY294002 was used to determine the relationship between USP18 and AKT in cervical cancer cells. Importantly, LY294002 significantly abolished the effects of USP18 overexpression in cervical cancer cells. In vivo, USP18 silencing inhibited human cervical cancer cells’ tumorigenicity. Conclusions The current study indicates that USP18 is an oncogenic gene in cervical cancer. Our findings not only deepened the understanding of USP18’s biological function in cervical cancer pathogenesis, but we also provided novel insight for cervical cancer therapy. Trial registration Retrospectively registered.

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Downregulation of TMOD1 promotes cell motility and cell proliferation in cervical cancer cells.

Publications

Downregulation of TMOD1 promotes cell motility and cell proliferation in cervical cancer cells.

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