ArticleAmerican journal of cancer research2020
SHCBP1 regulates STAT3/c-Myc signaling activation to promote tumor progression in penile cancer.
Article in American journal of cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Construction of a lncRNA-mediated ceRNA network and a genomic-clinicopathologic nomogram to predict survival for breast cancer patients.Cancer biomarkers : section A of Disease markers · 2023Trial
- The Roles of SHCBP1 in Cancer Hallmarks: Molecular Mechanisms and Therapeutic Implications.International journal of molecular sciences · 2025Review
- SHCBP1 contributes to the proliferation and self‑renewal of cervical cancer cells and activation of the NF‑κB signaling pathway through EIF5A.Oncology letters · 2023Article
- BP‑1‑102 exerts antitumor effects on T‑cell acute lymphoblastic leukemia cells by suppressing the JAK2/STAT3/c‑Myc signaling pathway.Experimental and therapeutic medicine · 2023Article
- Review
- Article
- RGS20 Promotes Tumor Progression through Modulating PI3K/AKT Signaling Activation in Penile Cancer.Journal of oncology · 2022Article
- Identification of SHCBP1 as a potential biomarker involving diagnosis, prognosis, and tumor immune microenvironment across multiple cancers.Computational and structural biotechnology journal · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A challenge in developing novel strategies for penile cancer (PC) is the limited understanding of the regulatory mechanisms involved in PC development. This study aims to examine the expression of SHC SH2 Domain-Binding Protein 1 (SHCBP1) in PC and to explore its oncogenic function. Aberrant SHCBP1 expression was observed in PC tissues compared with normal penile tissues. SHCBP1 expression was significantly associated with the pathological grade, T stage, nodal status, and pelvic lymph node metastasis, and could serve as an independent factor for unfavorable overall survival in PC. Manipulation of SHCBP1 expression affected cell proliferation, soft agar clonogenesis, and cell migration and invasion in PC cell lines. Moreover, we identified STAT3/c-Myc signaling as a potential downstream target of SHCBP1. SHCBP1 interacted with JAK2 and STAT3 upon EGF stimulation, which might regulate STAT3/c-Myc signaling activation in PC cells. Disruption of STAT3/c-Myc signaling attenuated cell proliferation and cell migration/invasion in PC cell lines. Nevertheless, overexpression of constitutively activated STAT3 or c-Myc rescued cell proliferation and cell migration/invasion caused by SHCBP1 depletion in PC cell lines. Consistently, SHCBP1 depletion attenuated STAT3/c-Myc signaling and suppressed tumor growth in a murine xenograft model. Importantly, correlated expression of SHCBP1, p-STAT3, and c-Myc was observed in PC tissues, confirming the clinical relevance of SHCBP1/STAT3/c-Myc signaling in PC. In conclusion, aberrant SHCBP1 expression could serve as a potential prognostic biomarker for PC. SHCBP1 might activate the STAT3/c-Myc signaling pathway to promote tumor progression in PC, which may serve as a potential target for PC treatment.
Indexed as
Identifiers
33163262PMC7642648W3104518921What OpenQuestion holds
Registered trials
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