ArticleCell death & disease2018
The novel KLF4/PLAC8 signaling pathway regulates lung cancer growth.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 51 citations in OpenAlex.
- Krüppel-Like Factor 4, a Hub Gate for Cell Crosstalk in Tumor Microenvironment.Cancer medicine · 2026Review
- Bufalin inhibits immune escape in metastatic colorectal cancer by regulating M2 macrophage polarization.Apoptosis : an international journal on programmed cell death · 2025Article
- Lung disease in relation to unique monocyte-macrophage subpopulations induced by combined inhalant endotoxin and collagen-induced arthritis.Frontiers in immunology · 2025Article
- A risk score based on polyamine metabolism and chemotherapy-related genes predicts prognosis and immune cells infiltration of lung adenocarcinoma.Journal of cellular and molecular medicine · 2024Article
- Abnormal expression of Krüppel-like transcription factors and their potential values in lung cancer.Heliyon · 2024Review
- Article
- Comparative analyses of monocyte memory dynamics from mice to humans.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- PLAC8 contributes to the malignant behaviors of cervical cancer cells by activating the SOX4-mediated AKT pathway.Histochemistry and cell biology · 2023Article
- KLF4 transcription factor in tumorigenesis.Cell death discovery · 2023Review
- PLAC8 is an innovative biomarker for immunotherapy participating in remodeling the immune microenvironment of renal clear cell carcinoma.Frontiers in oncology · 2023Article
- MiR-135b-5p is an oncogene in pancreatic cancer to regulate GPRC5A expression by targeting transcription factor KLF4.Cell death discovery · 2022Article
- PLAC8 Overexpression Promotes Lung Cancer Cell Growth via Wnt/Journal of immunology research · 2022Article
- Multifaced roles of PLAC8 in cancer.Biomarker research · 2021Review
- Identification of Autophagy- and Ferroptosis-Related lncRNAs Functioned through Immune-Related Pathways in Head and Neck Squamous Carcinoma.Life (Basel, Switzerland) · 2021Article
- Clinical significance of CD34Frontiers of medicine · 2021Article
- PLAC8 promotes adriamycin resistance via blocking autophagy in breast cancer.Journal of cellular and molecular medicine · 2021Article
- Current research advances in microRNA-mediated regulation of Krüppel-like factor 4 in cancer: a narrative review.Annals of translational medicine · 2021Review
- circUBAP2 exacerbates malignant capabilities of NSCLC by targeting KLF4 through miR-3182 modulation.Aging · 2021Observational
- STAT5a Confers Doxorubicin Resistance to Breast Cancer by Regulating ABCB1.Frontiers in oncology · 2021Article
- Polyphyllin Ⅲ-Induced Ferroptosis in MDA-MB-231 Triple-Negative Breast Cancer Cells can Be Protected Against by KLF4-Mediated Upregulation of xCT.Frontiers in pharmacology · 2021Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence suggests that placenta-specific 8 (PLAC8) plays an important role in normal cellular process and human diseases, including multiple types of human tumors, and its role is highly relied upon in cellular and physiologic contexts. However, there are no reports on its expression profile and biological roles during lung cancer development. In the current study, both the clinical implications and biological effects of PLAC8 in lung cancer (LC) progression were investigated, and we identified and described the novel Krüppel-like factor 4 (KLF4)/PLAC8 regulatory pathway in cancer progression. Elevated PLAC8 levels were positively correlated with tumor size, histological grade, and tumor node metasis (TNM) stage, and LC patients with high PLAC8 expression suffered poor outcomes. In vitro and in vivo assays further revealed that endogenous PLAC8 promoted cell proliferation and tumor formation. We also found downregulated PLAC8 protein in several LC cell lines following the induction of KLF4, and immunohistochemistry analysis of LC tissues by microarray indicated a potential inverse correlation between PLAC8 and KLF4 expression. Luciferase reporter analysis and chromatin immunoprecipitation assays determined that KLF4 negatively regulated PLAC8 promoter activity via directly binding to the promoter region. Furthermore, the growth inhibition resulting from KLF4 overexpression was partially rescued by ectopic PLAC8 expression. Together, our data uncovered a previously unidentified role of PLAC8 as a central mediator in LC progression. PLAC8 was transcriptionally repressed by KLF4, and the novel KLF4/PLAC8 axis may act as a promising candidate target for LC diagnosis and therapy.
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