ArticleBiochemical genetics2024
GABRP Promotes the Metastasis of Pancreatic Cancer by Activation of the MEK/ERK Signaling Pathway.
Article in Biochemical genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 37 citations in OpenAlex.
- GABRP Mediates GABA-A Receptor to Shape Tumor Immunosuppressive Microenvironment and Promote Tumor Immune Escape and Corresponding Targeted Therapy.Cancer medicine · 2025Article
- GABAMolecular cell · 2025Article
- The double role of GABAergic system in systemic tumors: an updated review.Frontiers in oncology · 2025Review
- Expression of gamma-aminobutyric acid type A receptor subunit π and minichromosome maintenance-3 in breast cancer patients treated with neoadjuvant chemotherapy: a target molecule or a proliferation marker?Revista da Associacao Medica Brasileira (1992) · 2025Article
- Elevated expression of Aurora-A/AURKA in breast cancer associates with younger age and aggressive features.Breast cancer research : BCR · 2024Article
- GABRP inhibits the progression of oesophageal cancer by regulating CFTR: Integrating bioinformatics analysis and experimental validation.International journal of experimental pathology · 2024Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic cancer remains the common cancer with the worst prognosis because of its late diagnosis and extensive metastasis. This study aimed to investigate the effects of GABRP on pancreatic cancer metastasis and the molecular mechanism. The expression of GABRP was measured using the quantitative real-time PCR and western blot. The biological behaviors of cancer cells were assessed using the cell counting kit-8, Transwell assay, and western blot. The regulation of GABRP on the MEK/ERK pathway was detected by western blot. The results indicated that GABRP was overexpressed in pancreatic cancer tissues and cells. Knockdown of GABRP suppressed cell viability, invasion, migration, and epithelial-mesenchymal transition (EMT), whereas GABRP overexpression facilitated these biological behaviors. Inactivation of the MEK/ERK pathway reversed the effects on cellular processes induced by GABRP. Moreover, silencing of GABRP inhibited tumor growth. In conclusion, GABRP promoted the progression of pancreatic cancer by facilitating cell metastasis and tumor growth via activating the MEK/ERK pathway. The findings suggest that GABRP has the potential to be a therapeutic target for the metastatic pancreatic cancer.
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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.