Knocking-down of CREPT prohibits the progression of oral squamous cell carcinoma and suppresses cyclin D1 and c-Myc expression

Ma, Junxun; Ren, Yipeng; Zhang, Lei; Kong, Xiangpan; Wang, Tong; Shi, Yueyi; Bu, Rongfa

doi:10.1371/journal.pone.0174309

Cited by 23 publications

(17 citation statements)

References 26 publications

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“…Knockdown of CREPT inhibits the proliferation and migration of non-small cell lung cancer cells, whereas overexpression of CREPT demonstrates an oncogenic effect (21,43). Similarly, an oncogenic function of CREPT has been observed in oral squamous cell carcinoma and gastric cancer (22,44). Notably, CREPT has been reported to be highly expressed in HCC tissues and cell lines (16).…”

Section: Discussionmentioning

confidence: 80%

“…A high expression level of CREPT is correlated with tumor stage, metastasis and a poor survival rate (19–21). Previous studies have demonstrated that CREPT promotes tumor growth in vivo and in vitro by accelerating cell growth and cell cycle progression (22,23). Therefore, CREPT may serve as a potential and promising target for the development of anticancer treatments.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA‑300 inhibits the growth of hepatocellular carcinoma cells by downregulating CREPT/Wnt/β‑catenin signaling

Bai

Gao

et al. 2019

Oncol Lett

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A number of studies have demonstrated that altered expression levels of microRNA-300 (miR-300) are associated with tumor progression; however, little is understood regarding the role of miR-300 in hepatocellular carcinoma (HCC). The present study aimed to investigate the expression, biological function and potential regulatory mechanism of miR-300 in HCC. A miR-300 mimic and miR-300 inhibitor were transfected into liver cancer cells using RNAiMAX reagent. The expression levels of miR and mRNA were detected by reverse transcription-quantitative polymerase chain reaction. Protein expression levels were detected by western blot analysis. Cell growth was determined using Cell Counting Kit-8, a colony formation assay and cell cycle assay. miRNA targeting sites were analyzed using bioinformatics analysis and dual-luciferase reporter assay. The results revealed that miR-300 expression was significantly decreased in HCC tissues and cell lines. In vitro experiments demonstrated that overexpression of miR-300 could inhibit cell proliferation, colony formation and cell cycle progression of liver cancer cells. By contrast, inhibition of miR-300 was associated with increased rates of cell proliferation, colony formation and cell cycle progression. Notably, regulation of nuclear pre-mRNA domain-containing protein 1B (CREPT) was identified as a putative target gene of miR-300 by bioinformatics analysis. A luciferase reporter assay revealed that miR-300 directly targets the 3′-untranslated region of CREPT. Further data demonstrated that miR-300 can regulate CREPT expression levels in liver cancer cells. Notably, miR-300 was identified to regulate the Wnt/β-catenin signaling pathway in liver cancer cells. The restoration of CREPT expression partially reversed the antitumor effect of miR-300. In conclusion, the current results revealed a tumor suppressive role of miR-300 in HCC and indicated that the underlying mechanism was associated with a regulation of CREPT. The present study suggests that miR-300 and CREPT may serve as potential therapeutic targets for liver cancer.

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Section: Discussionmentioning

confidence: 80%

Section: Introductionmentioning

confidence: 99%

MicroRNA‑300 inhibits the growth of hepatocellular carcinoma cells by downregulating CREPT/Wnt/β‑catenin signaling

Bai

Gao

et al. 2019

Oncol Lett

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“…The protein expression levels of Wnt target genes including cyclin D1, VEGF, c-myc and survivin were enhanced after CIH treatment in a mouse model of lung cancer [21][22][23][24] . Cyclin D1 regulates the cell cycle by controlling G1/S transition, and the up-regulation of cyclin D1 is related to the development of various cancers 42,43 . C-Myc is an oncogenic transcription factor, recognizing E-box and related sequences in the promoters of target genes.…”

Section: Discussionmentioning

confidence: 99%

Intermittent hypoxia exacerbates tumor progression in a mouse model of lung cancer

Kang

Kwon

Kim

et al. 2020

Sci Rep

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the purpose of this study was to evaluate whether obstructive sleep apnea (oSA)-related chronic intermittent hypoxia (CIH) influences lung cancer progression and to elucidate the associated mechanisms in a mouse model of lung cancer. C57/BL6 mice in a CIH group were exposed to intermittent hypoxia for two weeks after tumor induction and compared with control mice (room air). Hypoxia inducible factor 1α (HIF-1α), vascular endothelial growth factor (VeGf) and metastasis-related matrix metalloproteinases (MMp) were measured. the expression levels of several hypoxia-related pathway proteins including HIF-1α, Wnt/ß-catenin, the nuclear factor erythroid 2-related factor 2 (Nrf2) and mammalian target of rapamycin-eRK were measured by western blot. the number (p < 0.01) and volume (p < 0.05) of tumors were increased in the CIH group. The activity of MMP-2 was enhanced after CIH treatment. The level of VEGF was increased significantly in the CIH group (p < 0.05). ß-catenin and Nrf2 were translocated to the nucleus and the levels of downstream effectors of Wnt/ß-catenin signaling increased after iH exposure. ciH enhanced proliferative and migratory properties of tumors in a mouse model of lung cancer. ß-catenin and Nrf2 appeared to be crucial mediators of tumor growth. Obstructive sleep apnea (OSA) is characterized by recurrent occlusion of the upper airway during sleep leading to chronic intermittent hypoxia (CIH). OSA is a highly prevalent sleep disorder affecting at least 3% to 7% of the adult population 1. OSA has been shown to be associated with morbidities including metabolic syndrome, systemic hypertension, pulmonary vascular disease, ischemic heart disease and congestive heart failure 2. In addition, OSA-related CIH has been suggested to affect tumor development and progression 3. OSA has been implicated in the increasing incidence of certain types of solid malignancies. In a Spanish cohort, increased overnight hypoxia as a surrogate of OSA severity was associated with increased cancer incidence in selected populations 4-6. Also, OSA was associated with increased cancer mortality in a community-based sample 7. The association between OSA and lung cancer has been evaluated. OSA-related CIH induced resistance to apoptosis and increased metastasis in lung cancer cells, in a manner related to hypoxia inducible factor 1α (HIF-1α) 8. The role of immune cells has been suggested as a potential mechanism linking OSA and cancer. Almendros et al. demonstrated that CIH induced changes in host immune responses are related to adverse cancer outcomes. CIH increases the mobilization of tumor-associated macrophages (TAMs) into tumors, and induces macrophages to transform from an anti-tumor phenotype (M1) to a tumor-promoting phenotype (M2) 9. Cyclooxygenase-2 inhibited IH-induced M2 polarization of TAMs and prevented IH-induced adverse tumor outcomes in a mouse model of sleep apnea 10. OSA-related CIH altered CD8 + T-cells in combination with changes in the tumor microenvironment that enhanced malignant tumor properties 11. Studies...

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“…Human oral keratinocyte (HOK) cells (ScienCell Research Laboratories, Carlsbad, CA, USA) were used as a normal control (28). The LSCC cell lines were grown in RPMI-1640 (Gibco; Thermo Fisher Scientific, Inc., Waltham, MA, USA; cat.…”

Section: Methodsmentioning

confidence: 99%

MicroRNA‑143‑3p suppresses cell growth and invasion in laryngeal squamous cell carcinoma via targeting the k‑Ras/Raf/MEK/ERK signaling pathway

zhang

Cao

2018

Int J Oncol

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MicroRNAs (miRNAs or miRs) have been identified as an important regulator in carcinogenesis and other pathological processes. However, the molecular mechanism underlying the function of miRNAs in the progression and development of laryngeal squamous cell carcinoma (LSCC) remains to be fully elucidated. In the present study, the miRNA expression pattern in LSCC tissues was profiled using miRNA microarray analysis. It was found that a large set of miRNAs are aberrantly expressed in LSCC tissues and that miR-143-3p was the most markedly downregulated compared with normal tissues. The low expression of miR-143-3p was associated with poor prognosis in LSCC. The overexpression of miR-143-3p repressed cellular proliferation and induced apoptosis in vitro, and inhibited tumor growth in vivo. The upregulation of miR-143-3p suppressed cell migration and invasion through inhibiting the epithelial-mesenchymal transition cascade. In addition, it was verified that the oncogene k-Ras is a target of miR-143-3p in LSCC cells, and the suppressive effects of miR-143-3p on LSCC cells were abrogated by the overexpression of k-Ras. It was also revealed that miR-143-3p may inhibit cell growth and metastasis through targeting the k-Ras/Raf/mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) signaling pathway. Taken together, the data indicated that the miR-143-3p/k-Ras/Raf/MEK/ERK axis serves a key regulator in the development and progression of LSCC, suggesting that miR-143-3p may be a potential prognostic biomarker and therapeutic target in the treatment of LSCC.

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Knocking-down of CREPT prohibits the progression of oral squamous cell carcinoma and suppresses cyclin D1 and c-Myc expression

Cited by 23 publications

References 26 publications

MicroRNA‑300 inhibits the growth of hepatocellular carcinoma cells by downregulating CREPT/Wnt/β‑catenin signaling

MicroRNA‑300 inhibits the growth of hepatocellular carcinoma cells by downregulating CREPT/Wnt/β‑catenin signaling

Intermittent hypoxia exacerbates tumor progression in a mouse model of lung cancer

MicroRNA‑143‑3p suppresses cell growth and invasion in laryngeal squamous cell carcinoma via targeting the k‑Ras/Raf/MEK/ERK signaling pathway

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