ArticleOncotarget2017
The small heat shock protein B8 (HSPB8) modulates proliferation and migration of breast cancer cells.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
31 citing papers in PubMed, 53 citations in OpenAlex.
- FAK signaling pathways are modulated by HSPB8 and BAG3 in breast cancer.Cell communication and signaling : CCS · 2026Article
- Estrogen receptor β target gene expression reveals novel repressive functions in aggressive breast cancer.NPJ breast cancer · 2026Article
- Recognition of HSPB8 as a potential therapeutic target for prostate cancer.Frontiers in genetics · 2025Article
- HSPB8 binding to c-Myc alleviates hypoxia/reoxygenation-induced trophoblast cell dysfunction.Experimental and therapeutic medicine · 2024Article
- Article
- HSPB8 Facilitates the Oncogenesis and Advancement of Bladder Cancer via Activation of HSP27.Journal of Cancer · 2024Article
- Macrophage-specific autophagy-related gene HSPB8 is involved in the macrophage polarization in atherosclerosis.BMC cardiovascular disorders · 2023Article
- Identification of a six-gene signature to predict survival and immunotherapy effectiveness of gastric cancer.Frontiers in oncology · 2023Article
- HSPB8 counteracts tumor activity of BRAF- and NRAS-mutant melanoma cells by modulation of RAS-prenylation and autophagy.Cell death & disease · 2022Article
- The Role of Small Heat Shock Proteins in Protein Misfolding Associated Motoneuron Diseases.International journal of molecular sciences · 2022Review
- HSPB8 is a Potential Prognostic Biomarker that Correlates With Immune Cell Infiltration in Bladder Cancer.Frontiers in genetics · 2022Article
- Five crucial prognostic-related autophagy genes stratified female breast cancer patients aged 40-60 years.BMC bioinformatics · 2021Article
- The Role of HSPB8, a Component of the Chaperone-Assisted Selective Autophagy Machinery, in Cancer.Cells · 2021Review
- Retinoic Acid Downregulates HSPB8 Gene Expression in Human Breast Cancer Cells MCF-7.Frontiers in oncology · 2021Article
- DNAJC12 as a Mediator Between ESR1 and ERBB4 in Breast Carcinoma Cells.Frontiers in oncology · 2021Article
- The involvement of small heat shock protein in chemoresistance in ovarian cancer -EXCLI journal · 2021Article
- FRL: An Integrative Feature Selection Algorithm Based on the Fisher Score, Recursive Feature Elimination, and Logistic Regression to Identify Potential Genomic Biomarkers.BioMed research international · 2021Article
- Heat shock protein B8 promotes proliferation and migration in lung adenocarcinoma A549 cells by maintaining mitochondrial function.Molecular and cellular biochemistry · 2021Article
- Small Heat Shock Proteins in Cancers: Functions and Therapeutic Potential for Cancer Therapy.International journal of molecular sciences · 2020Review
- The Role of Sex and Sex Hormones in Neurodegenerative Diseases.Endocrine reviews · 2020Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer (BC) is one of the major causes of cancer death in women and is closely related to hormonal dysregulation. Estrogen receptor (ER)-positive BCs are generally treated with anti hormone therapy using antiestrogens or aromatase inhibitors. However, BC cells may become resistant to endocrine therapy, a process facilitated by autophagy, which may either promote or suppress tumor expansion. The autophagy facilitator HSPB8 has been found overexpressed in some BC. Here we found that HSPB8 is highly expressed and differentially modulated by natural or synthetic selective ER modulators (SERMs), in the triple-positive hormone-sensitive BC (MCF-7) cells, but not in triple-negative MDA-MB-231 BC cells. Specific SERMs induced MCF-7 cells proliferation in a HSPB8 dependent manner whereas, did not modify MDA-MB-231 cell growth. ER expression was unaffected in HSPB8-depleted MCF-7 cells. HSPB8 over-expression did not alter the distribution of MCF-7 cells in the various phases of the cell cycle. Conversely and intriguingly, HSPB8 downregulation resulted in an increased number of cells resting in the G0/G1 phase, thus possibly reducing the ability of the cells to pass through the restriction point. In addition, HSPB8 downregulation reduced the migratory ability of MCF-7 cells. None of these modifications were observed, when another small HSP (HSPB1), also expressed in MCF-7 cells, was downregulated. In conclusion, our data suggest that HSPB8 is involved in the mechanisms that regulate cell cycle and cell migration in MCF-7 cells.
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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.