miR-182 contributes to cell proliferation, invasion and tumor growth in colorectal cancer by targeting DAB2IP

Li, Xiaoli; Zhang, Xudong; Zhang, Qiuge; Lin, Rui

doi:10.1016/j.biocel.2019.04.002

Cited by 28 publications

(31 citation statements)

References 37 publications

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“…MicroRNA (miR)-182 has been reported to act as an oncogene or tumor suppressor by regulating cell processes including proliferation, cell cycle, apoptosis, migration and invasion in different cancers because of the varying microenvironment. 10,11 Furthermore, previous studies demonstrate that miR-182 displays the suppressive role in gastric cancer development. [12][13][14] Rho-associated protein kinase 1 (ROCK1) is an important oncogene in human cancers, including gastric cancer.…”

Section: Introductionmentioning

confidence: 99%

<p>Down-Regulation of circNRIP1 Promotes the Apoptosis and Inhibits the Migration and Invasion of Gastric Cancer Cells by miR-182/ROCK1 Axis</p>

Liang

2020

OTT

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Aim: Circular RNAs (circRNAs) play important roles in the progression of human cancers. circRNA nuclear receptor interacting protein 1 (circNRIP1) has been reported to play as an oncogene in gastric cancer. However, the mechanism underlying circNRIP1 in gastric cancer progression is far from understood. Patients and Methods: Forty-five gastric cancer patients were recruited and overall survival of patients was analyzed. Gastric cancer cell lines MGC-803 and AGS cells were cultured for study in vitro. The expression levels of circNRIP1, microRNA (miR)-182 and rho-associated protein kinase 1 (ROCK1) were detected by quantitative real-time polymerase chain reaction or Western blot. Cell migration, invasion, cell cycle distribution and apoptosis were determined by transwell, flow cytometry and Western blot assays, respectively. The target association between miR-182 and circNRIP1 or ROCK1 was assessed by luciferase reporter assay and RNA immunoprecipitation. Results: circNRIP1 expression was enhanced in gastric cancer tissues and cells and high expression of circNRIP1 indicated poor survival of patients. Knockdown of circNRIP1 suppressed cell migration and invasion, arrested cell cycle at G0-G1 phase and promoted apoptosis in gastric cancer cells. miR-182 was a target of circNRIP1 and its deficiency reversed the effect of circNRIP1 silence on cell migration, invasion, cell cycle distribution and apoptosis in gastric cancer cells. Moreover, ROCK1 was validated as a target of miR-182 and competitively regulated by circNRIP1. Conclusion: Silence of circNRIP1 inhibited progression of gastric cancer by increasing miR-182 and decreasing ROCK1, providing a novel target for the treatment of gastric cancer.

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Section: Introductionmentioning

confidence: 99%

<p>Down-Regulation of circNRIP1 Promotes the Apoptosis and Inhibits the Migration and Invasion of Gastric Cancer Cells by miR-182/ROCK1 Axis</p>

Liang

2020

OTT

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“…Upregulated miR-1258 directly targets E2F8 to regulate cell cycle and inhibit cell proliferation in CRC 36 . MiR-182 facilitated cell proliferation and tumor growth in CRC by modulating DAB2IP 37 . In our study, miR-4262 and miR-185-5p was found to be able to interact with circAGFG1 and YY1.…”

Section: Discussionmentioning

confidence: 99%

CircAGFG1 drives metastasis and stemness in colorectal cancer by modulating YY1/CTNNB1

et al. 2020

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Colorectal cancer (CRC) is a common malignancy with high occurrence and mortality worldwide. In recent years, the overall survival rate of CRC patients has been improved because of the advances in early diagnosis and therapy. However, the prognosis of CRC patients at the advanced stage is still poor due to high recurrence rate and metastasis. The function of circular RNA (circRNA) ArfGAP with FG repeats 1 (circAGFG1) has been explored in non-small-cell lung cancer and triple-negative breast cancer. Nevertheless, its role in CRC is not clear. In this study, circAGFG1 was upregulated in CRC cell lines. CircAGFG1 silencing significantly suppressed cell proliferation, migration, invasion, and stemness, while promoted cell apoptosis in CRC. Meanwhile, we found that circAGFG1 also accelerated CRC tumor growth and metastasis in vivo. Importantly, circAGFG1 activated Wnt/β-catenin pathway through regulating CTNNB1. Afterwards, YY1 was found to transcriptionally activate CTNNB1. Furthermore, circAGFG1 directly sponged miR-4262 and miR-185-5p to upregulate YY1 expression. Eventually, rescue assays demonstrated that the effect of circAGFG1 silencing on CRC cell functions was observably reversed by upregulating YY1 or CTNNB1. In brief, our findings uncovered that circAGFG1 modulated YY1/CTNNB1 axis to drive metastasis and stemness in CRC by sponging miR-4262 and miR-185-5p.

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“…The hypoxia-inducible miR-182 was reported to target two different RasGAPs: RASA1 in hepatocellular cancer and oral cavity squamous cells carcinoma, and DAB2IP in colorectal carcinoma [ 77 , 78 , 79 ]. Interestingly, miR-182-mediated RASA1 inactivation could also promote tumor vascularization by reprogramming the secretome of cancer cells: in fact, HUVECs (human umbilical vein endothelial cells) treated with culture medium from RASA1-depleted cells showed increased capillary-like structure formation [ 77 ].…”

Section: Post-transcriptional Inhibition Of Rasgaps In Cancermentioning

confidence: 99%

Cutting the Brakes on Ras—Cytoplasmic GAPs as Targets of Inactivation in Cancer

Bellazzo

Collavin

2020

Cancers

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The Ras pathway is frequently deregulated in cancer, actively contributing to tumor development and progression. Oncogenic activation of the Ras pathway is commonly due to point mutation of one of the three Ras genes, which occurs in almost one third of human cancers. In the absence of Ras mutation, the pathway is frequently activated by alternative means, including the loss of function of Ras inhibitors. Among Ras inhibitors, the GTPase-Activating Proteins (RasGAPs) are major players, given their ability to modulate multiple cancer-related pathways. In fact, most RasGAPs also have a multi-domain structure that allows them to act as scaffold or adaptor proteins, affecting additional oncogenic cascades. In cancer cells, various mechanisms can cause the loss of function of Ras inhibitors; here, we review the available evidence of RasGAP inactivation in cancer, with a specific focus on the mechanisms. We also consider extracellular inputs that can affect RasGAP levels and functions, implicating that specific conditions in the tumor microenvironment can foster or counteract Ras signaling through negative or positive modulation of RasGAPs. A better understanding of these conditions might have relevant clinical repercussions, since treatments to restore or enhance the function of RasGAPs in cancer would help circumvent the intrinsic difficulty of directly targeting the Ras protein.

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miR-182 contributes to cell proliferation, invasion and tumor growth in colorectal cancer by targeting DAB2IP

Cited by 28 publications

References 37 publications

<p>Down-Regulation of circNRIP1 Promotes the Apoptosis and Inhibits the Migration and Invasion of Gastric Cancer Cells by miR-182/ROCK1 Axis</p>

<p>Down-Regulation of circNRIP1 Promotes the Apoptosis and Inhibits the Migration and Invasion of Gastric Cancer Cells by miR-182/ROCK1 Axis</p>

CircAGFG1 drives metastasis and stemness in colorectal cancer by modulating YY1/CTNNB1

Cutting the Brakes on Ras—Cytoplasmic GAPs as Targets of Inactivation in Cancer

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