ArticleHuman cell2021
Overexpression of SMC4 predicts a poor prognosis in cervical cancer and facilitates cancer cell malignancy phenotype by activating NF-κB pathway.
Article in Human cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- SMC4 is a hypoxia-responsive driver of pulmonary arterial hypertension through an HIF-1α-HDAC6-p21 regulatory axis.Respiratory research · 2026Article
- Superenhancer-driven SMC4 promotes myeloma growth by epigenetically enhancing IFI16-dependent STING signaling.Apoptosis : an international journal on programmed cell death · 2026Article
- NFIA-dependent upregulation of SMC4 promotes metastasis and metabolic reprogramming in glioma.Frontiers in oncology · 2025Article
- IL-32/NFκB/miR-205 loop sustains the high expression of IL-32 and enhances the motility of cervical cancer cells.Human cell · 2024Article
- FoxO1 promotes ovarian cancer by increasing transcription and METTL14-mediated mCancer science · 2024Article
- The TT Genotype of theCells · 2023Article
- Association ofAging · 2023Article
- Construction of a novel molecular typing and scoring system for anoikis distinguishes between different prognostic risks and treatment responsiveness in low-grade glioma.Frontiers in immunology · 2023Article
- SMC4, a novel tumor prognostic marker and potential tumor therapeutic target.Frontiers in oncology · 2023Review
- SMC4 serves as a potential marker for the diagnosis and prognosis of colon adenocarcinoma.International journal of immunopathology and pharmacologyArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cervical cancer is one of the leading female malignancy tumors worldwide. Structural maintenance of chromosomes 4 (SMC4), a member of the SMC family, is associated with cancer pathogenesis and progression. However, the role of SMC4 in cervical cancer is still unclear. In the study, SMC4 was increased in cervical cancer tissues compared with adjacent normal tissues. The SMC4 knockdown and overexpression were performed in cervical cancer cells. SMC4 knockdown inhibited cell proliferation, colony formation, cell migration and invasion, and suppressed epithelial-mesenchymal transition (EMT). Conversely, SMC4 overexpression exerted opposite effects. Moreover, SMC4 knockdown down-regulated stem cell markers, reduced the capacity of spheroid formation and inactivated NF-κB pathway. SMC4 overexpression contributed to stem cell markers, and stimulated spheroid formation and NF-κB pathway activation. Additionally, BAY11-7082 (an NF-κB inhibitor) alleviated the SMC4-mediated the effects in cervical cancer cells. In conclusion, these findings demonstrated that SMC4 overexpression facilitated the development of cervical cancer cells by activating NF-κBpathway, which provides a new therapeutic target for patients with cervical cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.