Colon Cancer

Shawki, Sherief; Ashburn, Jean; Signs, Steven A.; Huang, Emina

doi:10.1016/j.soc.2017.11.003

Cited by 77 publications

(35 citation statements)

References 84 publications

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“…The inflammatory response contributes to malignant tumor progression in the tumor microenvironment (25,26). Changes in the inflammatory microenvironment are frequently accompanied by molecular alternations in tumor tissues, and miRNAs are usually considered as potential mediators of these processes (27).…”

Section: Resultsmentioning

confidence: 99%

MicroRNA‑139‑5p regulates chronic inflammation by suppressing nuclear factor‑κB activity to inhibit cell proliferation and invasion in colorectal cancer

Zhu

Zhang

et al. 2019

Exp Ther Med

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The inflammatory microenvironment, which mediates the initiation and malignant development of tumors, has been reported to be associated with microRNA (miRNA) dysregulation. In the present study, the expression of miR-139-5p was analyzed in colorectal cancer (CRC) cell lines SW480, HT29, HCT-8, LoVo and HCT116, aiming to investigate the function and mechanism of miR-139-5p in the regulation of the malignant phenotypes of CRC. miR-139-5p expression was found to be considerably downregulated in CRC cell lines compared with the human normal colon mucosal epithelial cell line NCM460. Subsequently, it was demonstrated that overexpression of miR-139-5p in colon cancer cell lines significantly suppressed the cell proliferation in vitro and in vivo. In addition, overexpression of miR-139-5p further inhibited the invasion ability of colon cancer cells in vitro, concomitantly with downregulation of key invasion-associated proteins, including matrix metalloproteinase 9 (MMP9) and MMP7. Furthermore, it was demonstrated that overexpression of miR-139-5p decreased the expression levels of inflammatory cytokines, including interleukin-1β (IL-1β), IL-6 and tumor necrosis factor-α (TNF-α), by suppressing nuclear factor (NF)-κB activity. Therefore, these findings collectively indicated that miR-139-5p regulated chronic inflammation by suppressing NF-κB activity in order to inhibit cell proliferation and invasion in CRC, thereby indicating a novel molecular mechanism in CRC therapy.

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Section: Resultsmentioning

confidence: 99%

MicroRNA‑139‑5p regulates chronic inflammation by suppressing nuclear factor‑κB activity to inhibit cell proliferation and invasion in colorectal cancer

Zhu

Zhang

et al. 2019

Exp Ther Med

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“…2 During the past two decades, the incidence and mortality of CRC in Chinese are increased. 3 The common risk factors of CRC are family history of CRC, 4 inflammatory bowel disease (IBD), 5 consumption of red and processed meat, 6 sedentary lifestyles, 7 smoking 8 and bibulosity. 9 The therapeutic strategies for CC mainly include surgical resection, radiotherapy, chemotherapy, targeted therapy, and immunotherapy.…”

Section: Introductionmentioning

confidence: 99%

<p>Long Noncoding RNA MALAT1 Promotes the Development of Colon Cancer by Regulating <em>miR-101-3p</em>/STC1 Axis</p>

Luan¹,

Li²,

Liu³

et al. 2020

OTT

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Purpose: Colon cancer (CC) is a leading cause of cancer-related deaths worldwide. This study aimed to clarify the effect of long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on CC progression and the potential mechanism. Methods: CC cell lines HCT116 and HT29 were selected for functional analysis. The expression of MALAT1, microRNA (miR)-101-3p, and stanniocalcin 1 (STC1) in CC tissues and cells were measured by quantitative reverse transcription PCR (qRT-PCR). Cell proliferation, apoptosis, migration and invasion were measured by Cell Counting Kit-8 (CCK-8), flow cytometry, wound scratch and transwell assay, respectively. The target relationships (MALAT1 and miR-101-3p, miR-101-3p and STC1) were validated by dual-luciferase reporter and RNA pull-down assay. Results: The expression of MALAT1 was elevated in CC tissues compared with adjacent normal tissues and was associated with lymph node metastasis, depth of invasion and tumor-nodemetastasis (TNM) stage. Up-regulation of MALAT1 promoted the proliferation, migration, and invasion and inhibited the apoptosis of CC cells; while MALAT1 knockdown exhibited opposite results. MiR-101-3p was a target of MALAT1, which was negatively regulated by MALAT1. Silencing of miR-101-3p reverses the anti-tumor effect of MALAT1 knockdown on CC cells. STC1 was a target of miR-101-3p, which was negatively regulated by miR-101-3p. Silencing of STC1 reverses the tumor promoting effects of MALAT1 up-regulation and miR-101-3p downregulation on CC cells. Conclusion: MALAT1 may function as an oncogene in CC progression by affecting the miR-101-3p/STC1 axis, providing a hopeful therapeutic option for CC.

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“…The progression of COAD is through a multi‐stage process, from normal mucosa to adenoma, and finally to carcinoma (Arnold et al, ; Mutch, ). With the progression of COAD, gene mutations such as TP53 , Ras , and Braf , and abnormal gene expressions including TROP2 , ABCG2 , and HIF‐1 , have been reported to play crucial roles (Hall, Morris, & Sun, ; Recio‐Boiles & Cagir, ; Shawki, Ashburn, Signs, & Huang, ). However, the progression of COAD involving complex gene‐mechanisms has not yet been clearly explored.…”

Section: Introductionmentioning

confidence: 99%

Identification of hub genes and construction of transcriptional regulatory network for the progression of colon adenocarcinoma hub genes and TF regulatory network of colon adenocarcinoma

Wei

Chen

Huang

et al. 2019

Journal Cellular Physiology

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The aim of this study was to identify key genes related to the progression of colon adenocarcinoma (COAD), and to investigate the regulatory network of hub genes and transcription factors (TFs). Dataset GSE20916 including 44 normal colon, 55 adenoma, and 36 adenocarcinoma tissue samples was used to construct co-expression networks via weighted gene co-expression network. Gene Ontology annotation and the Kyoto

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Colon Cancer

Cited by 77 publications

References 84 publications

MicroRNA‑139‑5p regulates chronic inflammation by suppressing nuclear factor‑κB activity to inhibit cell proliferation and invasion in colorectal cancer

MicroRNA‑139‑5p regulates chronic inflammation by suppressing nuclear factor‑κB activity to inhibit cell proliferation and invasion in colorectal cancer

<p>Long Noncoding RNA MALAT1 Promotes the Development of Colon Cancer by Regulating <em>miR-101-3p</em>/STC1 Axis</p>

Identification of hub genes and construction of transcriptional regulatory network for the progression of colon adenocarcinoma hub genes and TF regulatory network of colon adenocarcinoma

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