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Background: Breast cancer (BC) is the most prevalent malignancy in women. Potential therapeutic targets for BC are of great significance. In our previous study, we found that prenylated rab acceptor 1 domain family member 2 (PRAF2) is an oncogene in BC. However, the exact mechanism of PRAF2 in BC cancer promotion is still not fully understood.
Methods: Pan-cancer analysis of PRAF2 was performed in the TIMER, Kaplan‒Meier, UALCAN and GEPIA databases.The prognostic value of PRAF2 in BC was investigated in the GEPIA database. The influence of PRAF2 on immune infiltration in BC was analyzed in the TISIDE and TIMER databases. Finally, we validated the expression of PRAF2 in our institutional samples. After downregulating PRAF2 in two BC cell lines, we tested cell proliferation by CCK-8 and Wound healing assays.
Results: PRAF2 was highly expressed in various cancers, including BC, and in most BC cell lines. Higher expression of PRAF2 indicated poorer overall survival (OS) but not disease-free survival (DFS). Higher expression of PRAF2 is an independent prognostic factor in BC.PRAF2 is more highly expressed in BC than in the corresponding normal tissues. Downregulation of PRAF2 in BC can significantly inhibit viability and migration.
Conclusions: PRAF2 is highly expressed in various cancers, including BC. The expression of PRAF2 is related to Liquid-Liquid Phase Separation in BC. Finally, PRAF2 is upregulated in BC based on our institutional data. Downregulation of PRAF2 significantly inhibits cellular viability、migration in BC. PRAF2 may be a potential biomarker and therapeutic target for BC.
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http://dx.doi.org/10.1186/s12885-024-13258-7 | DOI Listing |
BMC Cancer
January 2025
Department of Thyroid and Breast Surgery, Yijishan Hospital, First Affiliated Hospital of Wannan Medical College, Zheshan West Rd No. 2, Wuhu , Anhui Province, 241001, China.
Background: Breast cancer (BC) is the most prevalent malignancy in women. Potential therapeutic targets for BC are of great significance. In our previous study, we found that prenylated rab acceptor 1 domain family member 2 (PRAF2) is an oncogene in BC.
View Article and Find Full Text PDFInt J Mol Sci
January 2024
Department of Internal Medicine, School of Medicine, Pusan National University, Yangsan 50612, Republic of Korea.
The progression of idiopathic pulmonary fibrosis (IPF) is diverse and unpredictable. We identified and validated a new biomarker for IPF progression. To identify a candidate gene to predict progression, we assessed differentially expressed genes in patients with advanced IPF compared with early IPF and controls in three lung sample cohorts.
View Article and Find Full Text PDFInt J Mol Sci
December 2023
CNRS, INSERM, Institut Cochin, Université Paris Cité, F-75014 Paris, France.
Exp Ther Med
December 2022
Department of Thyroid and Breast Surgery, Yijishan Hospital of Wannan Medical College, Wuhu, Anhui 241001, P.R. China.
Prenylated rab acceptor 1 domain family member 2 (PRAF2) acts as an oncogene and is closely related to the occurrence and development of various tumors. The present study aimed to clarify the functional relevance of PRAF2 in the biological behaviors of breast cancer by determining the expression of PRAF2 in breast cancer tissues and the corresponding adjacent tissues. The gene phenotypes of PRAF2 in patients with breast cancer in The Cancer Genome Atlas database were predicted using a cancer data online analysis website: The University of Alabama at Birmingham Cancer Data Analaysis Portal (UALCAN).
View Article and Find Full Text PDFCell Mol Life Sci
September 2022
Université Paris Cité, Institut Cochin, INSERM U1016, CNRS UMR 8104, 75014, Paris, France.
The endoplasmic reticulum exit of some polytopic plasma membrane proteins (PMPs) is controlled by arginin-based retention motifs. PRAF2, a gatekeeper which recognizes these motifs, was shown to retain the GABA-receptor GB1 subunit in the ER. We report that PRAF2 can interact on a stoichiometric basis with both wild type and mutant F508del Cystic Fibrosis (CF) Transmembrane Conductance Regulator (CFTR), preventing the access of newly synthesized cargo to ER exit sites.
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