ArticleJournal of cellular and molecular medicine2019
PLCA8 suppresses breast cancer apoptosis by activating the PI3k/AKT/NF-κB pathway.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 37 citations in OpenAlex.
- VCP at the crossroads of UPS and autophagy in cancer.Genes & diseases · 2027Review
- PLAC8 participates in the prognosis regulation of breast cancer by regulating the infiltration of immune cells in the tumor microenvironment.Frontiers in bioinformatics · 2026Article
- RPPH1 promotes the progression of High-Risk acute myeloid leukemia through NF-κB signaling and Th17 expression.Medical oncology (Northwood, London, England) · 2025Article
- UFMylation System: Biological Functions, Molecular Mechanisms, Diseases, and Drug Discovery.MedComm · 2025Review
- Single-cell transcriptome analysis of bronchoalveolar lavage during early SARS-CoV-2 infection.Microbiology spectrum · 2025Article
- Interaction between NF-κB and PLAC8 impairs autophagy providing a survival advantage to prostate cells transformed by cadmium.Science advances · 2025Article
- PLAC8 attenuates pulmonary fibrosis and inhibits apoptosis of alveolar epithelial cells via facilitating autophagy.Communications biology · 2025Article
- Modulation of the tumor microenvironment and mechanism of immunotherapy-based drug resistance in breast cancer.Molecular cancer · 2024Review
- Role of UFMylation in tumorigenesis and cancer immunotherapy.Frontiers in immunology · 2024Review
- microRNA-944 inhibits breast cancer cell proliferation and promotes cell apoptosis by reducing SPP1 through inactivating the PI3K/Akt pathway.Apoptosis : an international journal on programmed cell death · 2023Article
- PLAC8 contributes to the malignant behaviors of cervical cancer cells by activating the SOX4-mediated AKT pathway.Histochemistry and cell biology · 2023Article
- Modification of PLAC8 by UFM1 affects tumorous proliferation and immune response by impacting PD-L1 levels in triple-negative breast cancer.Journal for immunotherapy of cancer · 2022Article
- The biology of YAP in programmed cell death.Biomarker research · 2022Review
- HJURP regulates cell proliferation and chemo-resistance via YAP1/NDRG1 transcriptional axis in triple-negative breast cancer.Cell death & disease · 2022Article
- Ginsenoside CK, rather than Rb1, possesses potential chemopreventive activities in human gastric cancerFrontiers in pharmacology · 2022Article
- Multifaced roles of PLAC8 in cancer.Biomarker research · 2021Review
- Clinical significance of CD34Frontiers of medicine · 2021Article
- PLAC8 promotes adriamycin resistance via blocking autophagy in breast cancer.Journal of cellular and molecular medicine · 2021Article
- Regulation of tamoxifen sensitivity by the PLAC8/MAPK pathway axis is antagonized by curcumin-induced protein stability change.Journal of molecular medicine (Berlin, Germany) · 2021Article
- PLAC8 gene knockout increases the radio-sensitivity of xenograft tumors in nude mice with nasopharyngeal carcinoma by promoting apoptosis.American journal of translational research · 2021Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cysteine-rich lysosomal protein placenta-specific 8 (PLAC8), also called onzin, has been shown to be involved in many types of cancers, and its role is highly dependent on cellular and physiological contexts. However, the precise function of PLAC8 in breast cancer (BC) progression remains unclear. In this study, we investigated both the clinical significance and biological functions of PLAC8 in BC progression. First, high PLAC8 expression was observed in primary BC tissues compared with adjacent normal tissues through immunohistochemistry analysis. The results of in vitro and in vivo assays further confirmed that PLAC8 overexpression promotes cell proliferation and suppress BC cell apoptosis, whereas PLAC8 silencing has the opposite effect. In addition, the forced expression of PLAC8 greatly induces cell migration, partially by affecting the EMT-related genes, including down-regulating E-cadherin expression and facilitating vimentin expression. Further mechanistic analysis confirmed that PLAC8 contributes to cell proliferation and suppresses cell apoptosis in BC by activating the PI3K/AKT/NF-κB pathway. The results of our study provide new insights into an oncogenic role of PLAC8 and reveal a novel PLAC8/ PI3K/AKT/NF-κB pathway as a potential therapeutic target for BC.
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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.