Notch1 regulates tongue cancer cells proliferation, apoptosis and invasion

Gan, Rui‐Huan; Hua, Wei; Xie, Jing; Zheng, Danping; Lu, You‐Guang; Huang, Xiaoyu; Xie, Jian; Zhao, Yong; Ding, Lin‐Can; Su, Bogong; Lin, Lisong; Zheng, Dechun

doi:10.1080/15384101.2017.1395534

Cited by 58 publications

(52 citation statements)

References 31 publications

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“…NOTCH1 is involved in the regulation of the Akt/mTOR signaling pathway (46,47), which is widely acknowledged to promote cancer development (22)(23)(24)(25)(26)42). The present study revealed that shHSP27 decreased NOTCH1 expression, indicating that HSP27 might regulate chemoresistance in colon cancer cells via NOTCH1 and that NOTCH1 might regulate of HSP27 in the Akt/mTOR signaling pathway.…”

Section: Discussionsupporting

confidence: 49%

“…Furthermore, cross-talk among the notch receptor 1 (NOTCH1), mTOR and PI3K/Akt signaling pathways is associated with apoptosis (21). The binding of NOTCH1 to its ligands allows DNA-binding proteins to regulate the expression of NOTCH1 target genes, which are involved in the proliferation, differentiation and apoptosis of various tumor cells (22)(23)(24). Additionally, PI3K and its effectors, including Akt and mTOR, play a key role in the proliferation and survival of tumor cells (25).…”

Section: Introductionmentioning

confidence: 99%

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Role of HSP27 in the multidrug sensitivity and resistance of colon cancer cells

Liu

Long

et al. 2020

Oncol Lett

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Multidrug resistance in cancer cells is a primary factor affecting therapeutic efficacy. Heat shock 27 kD protein 1 (HSP27) is associated with cell apoptosis and resistance to chemotherapy. However, the mechanisms underlying HSP27-associated pathways in colon cancer cells remain unclear. Therefore, the present study used short hairpin (sh) RNA to inhibit HSP27 expression in colon cancer cells in order to investigate the effects in vitro and in vivo. Flow cytometry was used to investigate cell apoptosis and a xenograft model was employed to examine the tumorigenesis. Protein expression was measured by Western blotting. The results revealed that suppression of HSP27 expression significantly increased cell apoptosis, inhibited tumor growth and enhanced sensitivity to the anti-cancer agents 5-fluorouracil (5-FU) and vincristine (VCR). shHSP27 significantly decreased the expression of notch receptor 1 and the phosphorylation level of Akt and mTOR, and enhanced the effect of 5-FU and VCR. In conclusion, HSP27 suppression enhanced the sensitivity of colon cancer cells to 5-FU and VCR, and increased colon cancer cell apoptosis with and without chemotherapy. Therefore, the development of novel therapeutic agents that inhibit the expression of HSP27 may offer a new treatment option for colon cancer.

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Section: Discussionsupporting

confidence: 49%

Section: Introductionmentioning

confidence: 99%

Role of HSP27 in the multidrug sensitivity and resistance of colon cancer cells

Liu

Long

et al. 2020

Oncol Lett

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“…There are 41 genes with the most hemimethylation in tumor DNA, see Table 9. Among these genes, TP73 [18][19][20], GNAS [21][22][23][24][25], and NOTCH1 [26,27] are notable ones with known relations to cancer. Table 9 shows that among these 41 genes, 1 is a tumor suppressor (WT1), 3 are oncogenes (GNAS, NOTCh1, and PRDM16), and of those 3, 2 are translocated cancer genes (NOTCH1 and PRDM16).…”

Section: Resultsmentioning

confidence: 99%

Statistical and Bioinformatic Analysis of Hemimethylation Patterns in Lung Cancer

Sun

Zane

Fulton

et al. 2020

Preprint

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Background: DNA methylation is an epigenetic event involving the addition of a methyl-group to a cytosine-guanine base pair (i.e., CpG site). It is associated with different cancers. Our research focuses on studying lung cancer hemimethylation, which refers to methylation occurring on only one of the two DNA strands. Many studies often assume that methylation occurs on both DNA strands at a CpG site. However, recent publications show the existence of hemimethylation and its impact. It is important to identify cancer hemimethylation patterns. Methods: In this paper, we use the Wilcoxon signed rank test to identify hemimethylated CpG sites based on publicly available lung cancer methylation sequencing data. We then identify two types of hemimethylated CpG clusters, regular and polarity clusters, and genes with large numbers of hemimethylated sites. Highly hemimethylated genes are then studied for their biological interactions using available bioinformatics tools. Results: In this paper, we have conducted the first-ever in-depth investigation of hemimethylation for lung cancer. Our results show that hemimethylation does exist in lung cells either as singletons or clusters. Most clusters contain only 2 or 3 CpG sites. Polarity clusters are much shorter than regular clusters and appear less frequently. The majority of clusters found in tumor samples have no overlap with clusters found in normal samples, and vice versa. Several genes that are known to be associated with cancer are hemimethylated differently between the cancerous and normal samples. Furthermore, highly hemimethylated genes exhibit many different interactions with other genes that may be associated with cancer. Hemimethylation has diverse patterns and frequencies that are comparable between normal and tumorous cells. Therefore, hemimethylation may be related to both normal and tumor cell development. Conclusions: Our research has identified CpG clusters and genes that are hemimethylated in normal and lung tumor samples. Due to the potential impact of hemimethylation on gene expression and cell function, these clusters and genes may be important to advance our understanding of the development and progression of lung cancer.

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“…Notch1, a member of the Notch receptors, was predicted as a novel direct target gene of miR-495 in OSCC in the present study. Notch1 was reported to be overexpressed in OSCC, which was correlated with the T-stage, clinical stage, differentiation, lymph node metastasis, depth of invasion and locoregional recurrence (27)(28)(29). Notch1 activation has been reported to promote OSCC cell proliferation, apoptosis, migration, invasion and EMT (29)(30)(31).…”

Section: Discussionmentioning

confidence: 99%

“…3A). Notch1 was previously reported to be involved in the onset and progression of OSCC (27)(28)(29)(30)(31) and was therefore selected as a candidate for further confirmation in the present study. A luciferase reporter assay was performed to determine whether the 3'-UTR of Notch1 may be directly targeted by miR-495.…”

Section: Overexpression Of Mir-495 Prohibits the Proliferation And Inmentioning

confidence: 99%

MicroRNA‑495 targets Notch1 to prohibit cell proliferation and invasion in oral squamous cell carcinoma

Wang

Yang

et al. 2018

Mol Med Report

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MicroRNAs (miRNAs) are associated with the initiation and progression of oral squamous cell carcinoma (OSCC) by regulating a variety of cancer-associated behaviors. Fully understanding the regulatory mechanism of miRNAs in the pathogenesis of OSCC may provide novel promising approaches for the identification of prognostic biomarkers and therapeutic targets for this particular malignancy. In the present study, reverse transcription-quantitative polymerase chain reaction analysis was performed to detect miRNA (miR)-495 expression in OSCC tissues and cell lines. The effects of miR-495 on the proliferation and invasion of OSCC cells were determined using Cell Counting Kit-8 and Matrigel invasion assays, respectively. The mechanisms underlying the action of miR-495 in OSCC cells were also investigated. Results from the present study revealed that miR-495 expression was downregulated in OSCC tissues and cell lines compare with in adjacent normal tissues and human oral keratinocytes, respectively. Exogenous expression of miR-495 restricted cell proliferation and invasion of OSCC cells in vitro. Notch1 was identified as a direct functional target of miR-495 in OSCC. Furthermore, Notch1 knockdown exhibited inhibitory effects, similar to those induced by miR-495 overexpression in OSCC cells. Restoration of Notch1 expression rescued the suppressive effects of miR-495 on OSCC cell proliferation and invasion. These findings suggested an important role for miR-495 in the regulation of OSCC cell growth and metastasis, at least partly by directly targeting Notch1. In addition, the findings of the present study revealed the potential of miR-495 as a novel therapeutic target for the treatment of patients with OSCC.

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Notch1 regulates tongue cancer cells proliferation, apoptosis and invasion

Abstract: Our results prove that the oncogenic role of Notch1 in tongue cancer and provide the direction of targeted therapy of tongue cancer.

Cited by 58 publications

References 31 publications

Role of HSP27 in the multidrug sensitivity and resistance of colon cancer cells

Role of HSP27 in the multidrug sensitivity and resistance of colon cancer cells

Statistical and Bioinformatic Analysis of Hemimethylation Patterns in Lung Cancer

MicroRNA‑495 targets Notch1 to prohibit cell proliferation and invasion in oral squamous cell carcinoma

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