Proteomics

Dataset Information

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PLEKHA4 knockdown induces apoptosis in melanoma cells through the MAPK and cMyc signaling pathways


ABSTRACT: Melanoma, originating from the malignant transformation of melanocytes, is the deadliest form of skin cancer. The incidence of primary cutaneous melanoma is increasing, with about 132,000 new cases annually. While early-stage melanoma can often be treated successfully with surgery, advanced melanoma remains challenging, necessitating new therapeutic targets. The MAPK pathway, particularly involving MEK and ERK, is critical in melanoma progression. PLEKHA4, a protein involved in cancer biology, has been identified as a key factor in melanoma cell proliferation and progression. Our study investigated the role of PLEKHA4 in regulating MAPK signaling and its impact on drug sensitivity in melanoma. Proteomic analysis, cell culture experiments, and various molecular techniques, including immunoblotting and quantitative proteomics, were employed to elucidate PLEKHA4’s function. Results indicates that PLEKHA4 is overexpressed in melanoma, promoting cell proliferation. PLEKHA4 knockdown induces apoptosis through the MAPK and cMyc pathway. enhances cMyc ubiquitination and degradation, suggesting a potential mechanism for its role in melanoma. These findings highlight PLEKHA4 as a significant player in melanoma progression and a potential target for therapeutic intervention.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Melanocyte, Shoot

DISEASE(S): Skin Melanoma

SUBMITTER: Yuyang Yue  

LAB HEAD: Dongyuan Xu

PROVIDER: PXD053608 | Pride | 2025-01-22

REPOSITORIES: pride

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Publications

PLEKHA4 upregulation regulates KIRC cell proliferation through β‑catenin signaling.

Yue Yuyang Y   An Guangqi G   Cao Shuxia S   Li Xiangdan X   Du Liping L   Xu Dongyuan D   Jin Toufeng T   Liu Lan L  

Molecular medicine reports 20241114 1


In the present study, pleckstrin homology domain‑containing family A member 4 (PLEKHA4) was identified as being upregulated in renal cell carcinoma, particularly within the kidney renal clear cell carcinoma (KIRC) subtype. The present study conducted bioinformatics analysis, Cell Counting Kit‑8 and cell migration assays, flow cytometry, western blotting and <i>in vivo</i> experiments with the aim of uncovering the role of PLEKHA4 in β‑catenin signaling in KIRC cells. Notably, PLEKHA4 upregulatio  ...[more]

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