ArticleInfectious agents and cancer2017
HIV-1 matrix protein p17 and its variants promote human triple negative breast cancer cell aggressiveness.
Article in Infectious agents and cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Review
- ComparingCancers · 2025Article
- The association of HIV status with triple-negative breast cancer in patients with breast cancer in South Africa: a cross-sectional analysis of case-only data from a prospective cohort study.The Lancet. Global health · 2024Article
- HIV-1 Structural Proteins or Cell-Signaling Factors? That Is the Question!Current issues in molecular biology · 2024Review
- Navigating the Nexus: HIV and Breast Cancer-A Critical Review.International journal of molecular sciences · 2024Review
- The Persistence of HIV Diversity, Transcription, and Nef Protein in Kaposi's Sarcoma Tumors during Antiretroviral Therapy.Viruses · 2022Article
- Epidemiology of Breast Cancer Presentation in Botswana, South Africa, and the United States.The Journal of surgical research · 2022Article
- Long noncoding RNAs (lncRNAs) in HIV-mediated carcinogenesis: Role in cell homeostasis, cell survival processes and drug resistance.Non-coding RNA research · 2022Review
- B-cell clonogenic activity of HIV-1 p17 variants is driven by PAR1-mediated EGF transactivation.Cancer gene therapy · 2021Article
- Oncogenic Effects of HIV-1 Proteins, Mechanisms Behind.Cancers · 2021Review
- HIV-1 Reverse Transcriptase Promotes Tumor Growth and Metastasis Formation via ROS-Dependent Upregulation of Twist.Oxidative medicine and cellular longevity · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe introduction of cART has changed the morbidity and mortality patterns affecting HIV-infected (HIV
methodsWound-healing assay, matrigel-based invasion assay, and anchorage-independent proliferation assay were employed to compare the biological activity exerted by refp17 and three different vp17s on the triple-negative human breast cancer cell line MDA-MB 231. Intracellular signaling was investigated by western blot analysis.
resultsMotility and invasiveness increased in cells treated with both refp17 and vp17s compared to untreated cells. The effects of the viral proteins were mediated by binding to the chemokine receptor CXCR2 and activation of the ERK1/2 signaling pathway. However, vp17s promoted MDA-MB 231 cell growth and proliferation in contrast to refp17-treated or not treated cells.
conclusionsIn the context of the emerging role of the microenvironment in promoting and supporting cancer cell growth and metastatic spreading, here we provide the first evidence that exogenous p17 may play a crucial role in sustaining breast cancer cell migration and invasiveness, whereas some p17 variants may also be involved in cancer cell growth and proliferation.
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