Downregulation of miR-874-3p promotes chemotherapeutic resistance in colorectal cancer via inactivation of the Hippo signaling pathway

Que, Kaiqian; Tong, Yuanhe; Que, Ganbo; Li, Li; Lin, Hong-Cheng; Huang, Shuai; Wang, Ruo–Yu; Tang, Langlang

doi:10.3892/or.2017.6041

Cited by 31 publications

(35 citation statements)

References 80 publications

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“…Decreased miR-874 expression was associated with tumor-node-metastasis (TNM) stage, tumor size and lymph node metastasis in osteosarcoma (27). miR-874 expression levels were decreased in colorectal cancer and this downregulation exhibited a strong association with TNM stage and lymph node metastasis (28)(29)(30). In hepatocellular carcinoma, miR-874 expression levels were lower in tumor tissues and cell lines.…”

Section: Discussionmentioning

confidence: 99%

“…For instance, resumption expression of miR-874 suppressed osteosarcoma cell growth and metastasis, increased apoptosis in vitro and reduced tumour growth in vivo (27,34). Numerous studies have indicated that miR-874 upregulation inhibited cell proliferation, induced apoptosis and reversed chemoresistance in colorectal cancer (28)(29)(30). Que et al (30) and Leong et al (31) demonstrated that enforced expression of miR-874 inhibited cell proliferation, colony formation, metastasis and epithelial-mesenchymal transition, and promoted the apoptosis of hepatocellular carcinoma.…”

Section: Discussionmentioning

confidence: 99%

“…Numerous studies have indicated that miR-874 upregulation inhibited cell proliferation, induced apoptosis and reversed chemoresistance in colorectal cancer (28)(29)(30). Que et al (30) and Leong et al (31) demonstrated that enforced expression of miR-874 inhibited cell proliferation, colony formation, metastasis and epithelial-mesenchymal transition, and promoted the apoptosis of hepatocellular carcinoma. Jiang et al (33) and Zhang et al (35) reported that miR-874 overexpression repressed gastric cancer cell growth and metastasis and decreased angiogenesis in vitro and in vivo.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA‑874 inhibits proliferation and invasion of pancreatic ductal adenocarcinoma cells by directly targeting paired box 6

Diao

Cao

et al. 2018

Mol Med Report

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Studies have demonstrated that a number of microRNAs (miRNAs) are dysregulated in pancreatic ductal adenocarcinoma (PDAC), and alterations in their expression may affect the onset and progression of PDAC. Therefore, the expression patterns, biological functions and associated molecular mechanisms of miRNAs in PDAC should be elucidated for the development of novel therapeutic methods. Previous studies reported significant miRNA‑874 (miR‑874) dysregulation in multiple types of human cancer. However, the expression pattern, possible roles and underlying mechanisms of miR‑874 in PDAC remain to be elucidated. This study evaluated miR‑874 expression in PDAC and examined its biological functions and underlying mechanism of action in PDAC progression. miR‑874 expression was downregulated in PDAC tissues and cell lines. Functional experiments demonstrated that upregulation of miR‑874 inhibited cell proliferation and invasion in PDAC. Additionally, paired box 6 (PAX6) was predicted as a putative target of miR‑874 using bioinformatics analysis. Further experiments demonstrated that PAX6 may be the direct target gene of miR‑874 in PDAC. PAX6 knockdown exhibited similar inhibitory effects to miR‑874 overexpression in PDAC cells. In addition, restored PAX6 expression may reverse the suppressive roles of miR‑874 overexpression in PDAC cells. The results demonstrated that miR‑874 may serve tumor suppressive roles in PDAC by directly targeting PAX6. Therefore, miR‑874 may exhibit potential applications for treatment of patients with PDAC.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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MicroRNA‑874 inhibits proliferation and invasion of pancreatic ductal adenocarcinoma cells by directly targeting paired box 6

Diao

Cao

et al. 2018

Mol Med Report

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“…Hypoxia tumor microenvironment [37] and enhancement of autophagy procedure [38] both contribute to the chemoresistance of CRC cells. CRCs can also manipulate expression of multiple microRNAs to facilitate their chemoresistance, including suppressing expression of antitumor microRNAs, such as miR-181a/135a/302c [39], miR-874-3p [40], miR-200c [41]; and increasing tumorigenic miRNAs, such as miR-196b-5p [42], miR-315b [43], miR-10b [44].…”

Section: Conclusion and Discussionmentioning

confidence: 99%

“…Several cellular pathways were identified to abnormally modulated to facilitate CRC cells chemoresistant procedure, including activation of Wnt/β-catenin pathway [45], Akt pathway [46], and Notch signalling pathway [47], and inactivation of Hippo signalling pathway [40] and caspase-dependent apoptosis pathway [48]. Recently, it was identified that DCLK1 might be associated with chemoresistance of cancer cells.…”

Section: Conclusion and Discussionmentioning

confidence: 99%

Doublecotin-like kinase 1 increases chemoresistance of colorectal cancer cells through the anti-apoptosis pathway

Jones

Mei

2019

Preprint

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Colorectal cancer (CRC) is the third most common cancer diagnosed and the second leading cause of cancer-related deaths in the United States. About 50% of CRC patients relapsed after surgical resection and ultimately died of metastatic disease. Cancer stem cells (CSCs) are believed to be the primary reason for the recurrence of CRC. Specific stem cell marker, doublecortin-like kinase 1 (DCLK1) plays critical roles in initiating tumorigenesis, facilitating tumor progression, and promoting metastasis of CRC. It is up-regulated in CRC and upregulation of DCLK1 indicates poor prognosis. Whether DCLK1 is correlated with enhanced chemoresistance of CRC cells is unclear. Our research aims to reveal association of DCLK1 with chemoresistance of CRC cells and the underlying molecular mechanisms. In order to achieve our goal, we established stable DCLK1 over-expression cells (DCLK1+) using the HCT116 cells (WT). DCLK1+ and WT cells were treated with 5-Fluorouracil (5-Fu) at different doses for 24 or 48 hours. MTT assay was used to evaluate cell viability and IC 50 of 5-Fu was determined. Quantitative real time PCR was applied to determine gene expression of caspase-3 (casp-3), caspase-4 (casp-4), and caspase-10 (casp-10). Cleaved casp-3 expression was investigated using Western blot and immunofluorescence. Our results demonstrated that IC 50 of 5-Fu for the DCLK1+ cells was significantly higher than that of the WT cells for both 24 and 48hour treatment (P=0.002 and 0.048 respectively), indicating increased chemoresistance of the DCLK1+ cells. Gene expression of casp-3, casp-4, and casp-10 were significantly inhibited in the DCLK1+ cells after 5-Fu treatment compared to the WT cells (P=7.616e-08, 1.575e-05 and 5.307e-08, respectively). Cleaved casp-3 amount and casp-3 positive cells were significantly decreased in the DCLK1+ cells after 5-Fu treatment compared to the WT cells (P=0.015). In conclusion, our results demonstrated that DCLK1 overexpression enhanced the chemoresistance of CRC cells to 5-Fu treatment by suppressing gene expression of key caspases in the apoptosis pathway and activation of apoptosis pathway. DCLK1 can be an intriguing therapeutic target for the effective treatment of CRC patients.

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The direct miR‐874‐3p‐target FAM84A promotes tumor development in papillary thyroid cancer

Ding

et al. 2021

Molecular Oncology

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With the improvement of diagnostic technology, the incidence of thyroid cancer (TC) is on the rise. Papillary thyroid carcinoma (PTC) is the most common pathological type of thyroid cancer, therefore, it is important to explore some valuable molecular targets to improve the treatment and prognosis of PTC. Studies have shown that family with sequence similarity 84, member A (FAM84A) is involved in the development of various tumors. However, the role of FAM84A in PTC remains unknown. Herein, we explored the biological function and specific molecular mechanism of FAM84A in PTC. Results indicated that FAM84A was upregulated in PTC tissues and cells. In addition, patients with higher FAM84A expression tended to possess larger tumor size, higher lymph node metastasis rate and advanced TNM stage. Further studies indicated that downregulation of FAM84A could inhibit the development of PTC in vitro and in vivo by repressing the epithelial-mesenchymal transition (EMT) and Wnt/β-catenin signaling pathway. Moreover,

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Downregulation of miR-874-3p promotes chemotherapeutic resistance in colorectal cancer via inactivation of the Hippo signaling pathway

Cited by 31 publications

References 80 publications

MicroRNA‑874 inhibits proliferation and invasion of pancreatic ductal adenocarcinoma cells by directly targeting paired box 6

MicroRNA‑874 inhibits proliferation and invasion of pancreatic ductal adenocarcinoma cells by directly targeting paired box 6

Doublecotin-like kinase 1 increases chemoresistance of colorectal cancer cells through the anti-apoptosis pathway

The direct miR‐874‐3p‐target FAM84A promotes tumor development in papillary thyroid cancer

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