ArticleAmerican journal of cancer research2015
RECK impedes DNA repair by inhibiting the erbB/JAB1/Rad51 signaling axis and enhances chemosensitivity of breast cancer cells.
Article in American journal of cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- The Roles of the Membrane-Anchored Glycoprotein RECK in Animal Development, Tumor Suppression, and Beyond.Life (Basel, Switzerland) · 2026Review
- Article
- Inhibition of PFKFB3 induces cell death and synergistically enhances chemosensitivity in endometrial cancer.Oncogene · 2021Article
- The transcription co-factor JAB1/COPS5, serves as a potential oncogenic hub of human chondrosarcoma cellsAmerican journal of cancer research · 2021Article
- Metformin overcomes resistance to cisplatin in triple-negative breast cancer (TNBC) cells by targeting RAD51.Breast cancer research : BCR · 2019Article
- MiR-92a promotes the invasion and migration of colorectal cancer by targeting RECK.International journal of clinical and experimental pathology · 2019Article
- MicroRNA-221 promotes papillary thyroid carcinoma cell migration and invasion via targeting RECK and regulating epithelial-mesenchymal transition.OncoTargets and therapy · 2019Article
- The homologous recombination protein RAD51 is a promising therapeutic target for cervical carcinoma.Oncology reports · 2017Article
- Non-homologous End Joining Inhibitor SCR-7 to Exacerbate Low-dose Doxorubicin Cytotoxicity in HeLa Cells.Journal of cancer prevention · 2017Article
- miR-590-5p regulates gastric cancer cell growth and chemosensitivity through RECK and the AKT/ERK pathway.OncoTargets and therapy · 2016Article
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
The reversion-inducing cysteine-rich protein with kazal motif (RECK) is an endogenous matrix metalloproteinase (MMP) inhibitor and a tumor suppressor. Its expression is dramatically down-regulated in human cancers. Our recent results suggest a novel MMP-independent anti-cancer activity of RECK by inhibiting the erbB signaling. Activation of the erbB signaling is associated with chemotherapeutic resistance, however, whether RECK could modulate drug sensitivity is still unknown. Here we demonstrated that expression of RECK induced the activation of ATM and ATR pathways, and the formation of γ-H2AX foci in breast cancer cells. RECK inhibited the erbB signaling and attenuated the expression of the downstream molecules Jun activation domain-binding protein 1 (JAB1) and the DNA repair protein RAD51 to impede DNA repair and to increase drug sensitivity. Treatment of epidermal growth factor or over-expression of HER-2 effectively reversed the inhibitory effect of RECK. In addition, ectopic expression of JAB1 counteracted RECK-induced RAD51 reduction and drug sensitization. Our results elucidate a novel function of RECK to modulate DNA damage response and drug resistance by inhibiting the erbB/Jab1/RAD51 signaling axis. Restoration of RECK expression in breast cancer cells may increase sensitivity to chemotherapeutic agents.
Indexed as
Identifiers
26396917PMC4568777W2225643890What OpenQuestion holds
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.