Overexpression of placenta specific 8 is associated with malignant progression and poor prognosis of clear cell renal cell carcinoma

Shi, Liping; Xiao, Long; Heng, Baoli; Mo, Shijie; Chen, Weijun; Su, Zexuan

doi:10.1007/s11255-017-1578-y

Cited by 27 publications

(27 citation statements)

References 30 publications

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“…PLAC8 has been described as a tumor suppressor and a tumor promoter in different types of cancer. For example, PLAC8 overexpression promotes the tumorigenic transformation in clear-cell renal-cell carcinoma, lung cancer, colon cancer and breast cancer, but it also suppresses the proliferation of hepatocellular carcinoma cells (12)(13)(14)(15)(16)(17). In accordance with the latter finding, the present study identified that PLAC8 expression was significantly lower in OSCC cell lines compared with human oral epithelial cells.…”

Section: Discussionsupporting

confidence: 88%

PLAC8 inhibits oral squamous cell carcinogenesis and epithelial-mesenchymal transition via the Wnt/β-catenin and PI3K/Akt/GSK3β signaling pathways

Wang

Shang

et al. 2020

Oncol Lett

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Placenta-specific 8 (PLAC8) is closely associated with the proliferation, apoptosis and autophagy of several tumor cells. However, the expression and function of PLAC8 in oral squamous cell carcinoma (OSCC) remain unknown. Therefore, the present study investigated the function and mechanism of PLAC8 in OSCC. Reverse transcription-quantitative PCR and western blot analyses were performed to quantify the expression of PLAC8 in OSCC cell lines. The function of PLAC8 in OSCC was investigated via transfection, the Transwell and Cell Counting Kit-8 assays, immunofluorescence staining and western blotting. The results demonstrated that PLAC8 exspression was downregulated in OSCC cell lines. PLAC8 inhibited the cell proliferation in OSCC. In addition, PLAC8 restrained invasion and epithelialmesenchymal transition of OSCC cells. Furthermore, β-catenin helped to repress PLAC8 expression by regulating the Wnt/βcatenin and PI3K/Akt/GSK3β signaling pathways in OSCC cells. Collectively, the results of the present study suggest that PLAC8 acts as a tumor suppressor in OSCC by downregulating β-catenin.

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Section: Discussionsupporting

confidence: 88%

PLAC8 inhibits oral squamous cell carcinogenesis and epithelial-mesenchymal transition via the Wnt/β-catenin and PI3K/Akt/GSK3β signaling pathways

Wang

Shang

et al. 2020

Oncol Lett

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“…PLAC8 also acted as a novel biomarker in liver carcinoma 13 , and PLAC8 recovery could suppress PI3K/Akt/GSK3b/Wnt/β-catenin signaling to reduce cell proliferation 14 . Overexpression of PLAC8 was associated with the malignant progression and patients’ poor prognosis in clear-cell renal cell carcinoma 15 . All these intriguing findings elucidated a pivotal role of PLAC8 in cancer progression and development.…”

Section: Introductionmentioning

confidence: 95%

The novel KLF4/PLAC8 signaling pathway regulates lung cancer growth

et al. 2018

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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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“…To date, the results of several studies have strongly suggested that PLAC8 regulates cell division, differentiation and apoptosis. 9,18,19 To determine the biological function of PLAC8 in BC, we first evaluated the level of PLAC8 mRNA in 55 samples of BC and their corresponding adjacent tissues. The level of PLAC8 mRNA was increased in BC tumour tissues ( Figure 1A).…”

Section: Plac8 Expression Is Frequently Up-regulated In Breast Cancermentioning

confidence: 99%

PLCA8 suppresses breast cancer apoptosis by activating the PI3k/AKT/NF‐κB pathway

Mao

Chen

Jia

et al. 2019

J Cellular Molecular Medi

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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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Overexpression of placenta specific 8 is associated with malignant progression and poor prognosis of clear cell renal cell carcinoma

Abstract: Our findings suggest that PLAC8 may be a potential prognostic indicator and therapeutic target for ccRCC.

Cited by 27 publications

References 30 publications

PLAC8 inhibits oral squamous cell carcinogenesis and epithelial-mesenchymal transition via the Wnt/β-catenin and PI3K/Akt/GSK3β signaling pathways

PLAC8 inhibits oral squamous cell carcinogenesis and epithelial-mesenchymal transition via the Wnt/β-catenin and PI3K/Akt/GSK3β signaling pathways

The novel KLF4/PLAC8 signaling pathway regulates lung cancer growth

PLCA8 suppresses breast cancer apoptosis by activating the PI3k/AKT/NF‐κB pathway

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Overexpression of placenta specific 8 is associated with malignant progression and poor prognosis of clear cell renal cell carcinoma

Abstract: Our findings suggest that PLAC8 may be a potential prognostic indicator and therapeutic target for ccRCC.

Cited by 27 publications

References 30 publications

PLAC8 inhibits oral squamous cell carcinogenesis and epithelial-mesenchymal transition via the Wnt/&beta;-catenin and PI3K/Akt/GSK3&beta; signaling pathways

PLAC8 inhibits oral squamous cell carcinogenesis and epithelial-mesenchymal transition via the Wnt/&beta;-catenin and PI3K/Akt/GSK3&beta; signaling pathways

The novel KLF4/PLAC8 signaling pathway regulates lung cancer growth

PLCA8 suppresses breast cancer apoptosis by activating the PI3k/AKT/NF‐κB pathway

Contact Info

Product

Resources

About

PLAC8 inhibits oral squamous cell carcinogenesis and epithelial-mesenchymal transition via the Wnt/β-catenin and PI3K/Akt/GSK3β signaling pathways

PLAC8 inhibits oral squamous cell carcinogenesis and epithelial-mesenchymal transition via the Wnt/β-catenin and PI3K/Akt/GSK3β signaling pathways