MUC1 downregulation inhibits non‑small cell lung cancer progression in human cell lines

Xu, Tao; Li, Daowei; Wang, Hongmei; Zheng, Taohua; Wang, Guangqiang; Xin, Ying

doi:10.3892/etm.2017.5062

Cited by 18 publications

(14 citation statements)

References 26 publications

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“…Similar to our study, a previous study has found that silencing of MUC1 is able to inhibit cell proliferation though the activation of apoptosis pathways and the induction of apoptosis in PANC-1 cells [39]. Additionally, another study has indicated that silencing of MUC1 is capable of inhibiting the development of non-small cell lung cancer cells [17]. As for the role of MUC1 in OSCC, it could be explained by the following reasons.…”

Section: Discussionsupporting

confidence: 86%

“…MUC1 possesses a core protein mass of 120–225 kDa, which increases to 250–500 kDa with glycosylation [14–16]. MUC1 consists of two subunits, namely an N-terminal extracellular subunit (MUC1-N) together with a C-terminal transmembrane subunit (MUC1-C) [17]. It is reported that overexpression of MUC1 is able to induce anchorage independent growth and tumorigenicity [18].…”

Section: Introductionmentioning

confidence: 99%

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MUC1 gene silencing inhibits proliferation, invasion, and migration while promoting apoptosis of oral squamous cell carcinoma cells

Zhang

Chi

et al. 2019

Bioscience Reports

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The aim of the present study is to investigate the role of RNA interference in the inhibition of MUC1 gene expression in occurrence and metastasis of oral squamous cell carcinoma (OSCC) and its in-depth mechanisms. The OSCC and normal oral mucosa tissues, as well as normal oral epithelial cell line HOK and OSCC cell line SCC-4, Cal-27, TSCCA, Tca8113 were obtained to detect the expression of MUC1. Slug expression in OSCC and normal oral mucosa tissues was also determined. The OSCC cells were grouped to investigate the role of MUC1 gene silencing on proliferation, DNA replication, cell cycle distribution, apoptosis, colony formation ability, epithelial-mesenchymal transition (EMT), invasion, and migration of OSCC cells. We first found higher positive rate of MUC1 and Slug expression in OSCC tissues. Next, it was determined that higher expression of MUC1 was found in OSCC tissues and cells. Furthermore, silencing of MUC1 declined Slug expression, inhibited the proliferation, DNA replication, cell cycle progression, and EMT while inducing apoptosis of OSCC cells. Our study suggests that overexpression of MUC1 is found in OSCC, and MUC1 gene silencing could inhibit the proliferation, invasion, and migration while inducing apoptosis of OSCC cells.

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Section: Discussionsupporting

confidence: 86%

Section: Introductionmentioning

confidence: 99%

MUC1 gene silencing inhibits proliferation, invasion, and migration while promoting apoptosis of oral squamous cell carcinoma cells

Zhang

Chi

et al. 2019

Bioscience Reports

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“…MUC1 is a transmembrane glycoprotein that is aberrantly glycosylated in many cancers, including NSCLC. 253,254 MUC1 and PSCA CAR-T cells showed independent and synergistic antitumor efficacy in a patient-derived xenograft model of NSCLC. 255 The First People's Hospital in Hefei, China is completing a Phase I/ II study of MUC1-CAR T cells for patients with MUC1+ advanced refractory NSCLC (NCT02587689).…”

Section: Ctla-4 Antibodymentioning

confidence: 94%

Making cold malignant pleural effusions hot: driving novel immunotherapies

et al. 2019

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Malignant pleural effusions, arising from either primary mesotheliomas or secondary malignancies, heralds advanced disease and poor prognosis. Current treatments, including therapeutic thoracentesis and tube thoracostomy, are largely palliative. The immunosuppressive environment within the pleural cavity includes myeloid derived suppressor cells, T-regulatory cells, and dysfunctional T cells. The advent of effective immunotherapy with checkpoint inhibitors and adoptive cell therapies for lung cancer and other malignancies suggests a renewed examination of local and systemic therapies for this malady. Prior strategies reporting remarkable success, including instillation of the cytokine interleukin-2, perhaps coupled with checkpoint inhibitors, should be further evaluated in the modern era.

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“…VEGF promotes angiogenesis, regulates the apoptosis of vascular endothelial cells and alveolar epithelial cells and increases the permeability of blood vessels, which leads to sustained tumor growth. For example, Xu [ 33 ] studied the inhibitory effect of MUC1 on NSCLC cells and the results of western blotting indicated that MUC1 significantly reduced the levels of VEGF and VEGF-C proteins, indicating that MUC1 has an anti-angiogenic effect and can be used as a potential treatment for NSCLC. In the present study, the expression level of VEGF decreased significantly when the PAP concentration increased, indicating that PAP could inhibit tumor angiogenesis and inhibit tumor growth.…”

Section: Resultsmentioning

confidence: 99%

Anti-Proliferation Activity of a Decapeptide from Perinereies aibuhitensis toward Human Lung Cancer H1299 Cells

et al. 2019

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Perinereis aibuhitensis peptide (PAP) is a decapeptide (Ile-Glu-Pro-Gly-Thr-Val-Gly-Met-Met-Phe, IEPGTVGMMF) with anticancer activity that was purified from an enzymatic hydrolysate of Perinereis aibuhitensis. In the present study, the anticancer effect of PAP on H1299 cell proliferation was investigated. Our results showed that PAP promoted apoptosis and inhibited the proliferation of H1299 cells in a time- and dose-dependent manner. When the PAP concentration reached 0.92 mM, more than 95% of treated cells died after 72 h of treatment. Changes in cell morphology were further analyzed using an inverted microscope and AO/EB staining and flow cytometry was adopted for detecting apoptosis and cell cycle phase. The results showed that the early and late apoptosis rates of H1299 cells increased significantly after treatment with PAP and the total apoptosis rate was significantly higher than that of the control group. Moreover, after treatment with PAP, the number of cells in the S phase of cells was significantly reduced and the ability for the cells to proliferate was also reduced. H1299 cells were arrested in the G2/M phase and cell cycle progression was inhibited. Furthermore, the results of western blotting showed that nm23-H1 and vascular endothelial growth factor (VEGF) protein levels decreased in a dose-dependent manner, while the pro-apoptotic protein and anti-apoptotic protein ratios and the level of apoptosis-related caspase protein increased in a dose-dependent manner. In conclusion, our results indicated that PAP, as a natural marine bioactive substance, inhibited proliferation and induced apoptosis of human lung cancer H1299 cells. PAP is likely to be exploited as the functional food or adjuvant that may be used for prevention or treatment of human non-small cell lung cancer in the future.

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MUC1 downregulation inhibits non‑small cell lung cancer progression in human cell lines

Cited by 18 publications

References 26 publications

MUC1 gene silencing inhibits proliferation, invasion, and migration while promoting apoptosis of oral squamous cell carcinoma cells

MUC1 gene silencing inhibits proliferation, invasion, and migration while promoting apoptosis of oral squamous cell carcinoma cells

Making cold malignant pleural effusions hot: driving novel immunotherapies

Anti-Proliferation Activity of a Decapeptide from Perinereies aibuhitensis toward Human Lung Cancer H1299 Cells

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