ArticleMolecular cancer research : MCR2016
miR-138-Mediated Regulation of KINDLIN-2 Expression Modulates Sensitivity to Chemotherapeutics.
Article in Molecular cancer research : MCR, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 71 citations in OpenAlex.
- DHT-Induced lncRNA AC092718.4 Promotes Prostate Cancer Cell Proliferation via ceRNA Mechanism.Genes · 2026Article
- Molecular cargo of small EVs from NSCLC patient BALF and plasma: unveiling their role in airway inflammation and immune regulation in a novel human 3D bronchial model.Cell communication and signaling : CCS · 2025Article
- The Role of miR-138 in Cardiovascular Diseases.BioMed research international · 2025Review
- Kindlin-2 regulates the oncogenic activities of integrins and TGF-β in triple-negative breast cancer progression and metastasis.Oncogene · 2024Article
- Role of Kindlin 2 in prostate cancer.Scientific reports · 2024Article
- Pan-cancer analyses suggest kindlin-associated global mechanochemical alterations.Communications biology · 2024Article
- circCYP24A1 promotes Docetaxel resistance in prostate Cancer by Upregulating ALDH1A3.Biomarker research · 2022Article
- Article
- Role of noncoding RNA in drug resistance of prostate cancer.Cell death & disease · 2021Review
- Regulation of host and virus genes by neuronal miR-138 favours herpes simplex virus 1 latency.Nature microbiology · 2021Article
- Kindlins as modulators of breast cancer progression.Journal of breast cancer research · 2021Article
- The roles of integrins in cancer.Faculty reviews · 2021Review
- Comparison of Snail1, ZEB1, E-Cadherin Expression Levels in HPV-Induced Cervical Cancer.Iranian journal of public health · 2020Article
- Role of Kindlin-2 in cancer progression and metastasis.Annals of translational medicine · 2020Review
- The focal adhesion protein kindlin-2 controls mitotic spindle assembly by inhibiting histone deacetylase 6 and maintaining α-tubulin acetylation.The Journal of biological chemistry · 2020Article
- MicroRNA-138 inhibits tumor growth and enhances chemosensitivity in human cervical cancer by targeting H2AX.Experimental and therapeutic medicine · 2020Article
- The Kindlin2-p53-SerpinB2 signaling axis is required for cellular senescence in breast cancer.Cell death & disease · 2019Article
- Hypoxia-induced PIM kinase and laminin-activated integrin α6 mediate resistance to PI3K inhibitors in bone-metastatic CRPC.American journal of clinical and experimental urology · 2019Article
- The Kindlin-2 regulation of epithelial-to-mesenchymal transition in breast cancer metastasis is mediated through miR-200b.Scientific reports · 2018Article
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Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledProstate cancer is the second leading cause of cancer-related death in men, second only to lung cancer, mainly due to disease reoccurrence as a result to lack of response to androgen deprivation therapies (ADT) after castration. Patients with metastatic castration-resistant prostate cancer (mCRPC) have very limited treatment options, with docetaxel as the first-line standard of care, for which resistance to this chemotherapeutic ultimately develops. Therefore, finding ways to sensitize tumors to chemotherapies and to limit chemoresistance provides a viable strategy to extend the survival of mCRPC patients. This study investigated the role of Kindlin-2 (FERMT2/K2), a member of the Kindlin family of FERM domain proteins and key regulators of the adhesive functions mediated by integrin, in the sensitization of mCRPC to chemotherapeutics. Loss of K2, which is overexpressed in prostate cancer cells derived from mCRPC tumors, compared with those cells derived from androgen-dependent tumors, significantly enhanced apoptosis and cell death of docetaxel-treated PC3 cells. Furthermore, it was determined that K2-mediated sensitization to docetaxel treatment is the result of inhibition of β1-integrin signaling. Finally, miR-138 specifically targeted K2 and inhibited its expression, thereby regulating a miR-138/K2/β1-integrin signaling axis in mCRPC that is critical for the modulation of sensitivity to chemotherapeutics. Thus, these data identify a novel signaling axis where K2 in combination with chemotherapeutics provides a new target for the treatment of mCRPC. IMPLICATIONS: Targeted inhibition of Kindlin-2 in combination with chemotherapy represents an effective treatment option for mCRPC.
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