miR-26a and miR-26b inhibit esophageal squamous cancer cell proliferation through suppression of c-MYC pathway

Li, Juan; Yue, Liang; Lv, Hao; Meng, Hui; Xiong, Gang; Guan, Xingying; Chen, Xuedan; Bai, Yun; Wang, Kai

doi:10.1016/j.gene.2017.05.001

Cited by 73 publications

(62 citation statements)

References 28 publications

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“…Previous studies revealed that miR‐26a is involved in the development and progression of various cancers, and it is widely accepted that miR‐26a functions as a tumour suppressor and expression of miR‐26a was decreased in various tumour tissues, such as esophageal squamous cell carcinoma, prostate cancer and ovarian cancer . Li X et al and Li L et al reported that miR‐26a was reduced in LSCC tissues by microarray analysis; consistent with this, we determined that miR‐26a was down‐regulated in LSCC tissues and cell lines, suggesting miR‐26a may play an important role in LSCC development.…”

Section: Discussionsupporting

confidence: 87%

“…For example, miR‐300 inhibited cell proliferation and invasion via targeting ROS1 in Hep‐2 cells, miR‐203 played as a tumor suppressor by repressing proliferation, migration and invasion of Hep‐2 cells through the regulation of VEGFA and Cox‐2 . Multiple lines of evidence have indicated that miR‐26a plays a critical role in various cancer cells, including gastric carcinoma, melanoma, colorectal cancer, B‐cell lymphoma, esophageal squamous cancer . Additionally, according to microarray data of miR expression, miR‐26a was down‐regulated in LSCC tissues compared with adjacent non‐neoplastic tissues .…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA‐26a inhibits proliferation and tumorigenesis via targeting CKS2 in laryngeal squamous cell carcinoma

et al. 2018

Clin Exp Pharma Physio

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Laryngeal squamous cell carcinoma (LSCC) is one of the most common head and neck cancers, with high mortality and incidence. MicroRNA-26a (miR-26a) is involved in the development and progression of several tumours. However, the roles of miR-26a and its target CKS2 in LSCC progression are not yet clear. The mRNA and protein expression was determined using RT-PCR and Western blotting assay, respectively. Cell proliferation was detected using a Cell Counting kit-8 assay (CCK-8). Transwell assay was used to evaluate cell migration and invasion. Dual-luciferase reporter assay was applied to determine the relationship between miR-26a and CKS2. In addition, a tumour xenograft model in nude mice was established to further determine the effects of miR-26a on tumourigenesis. In this study, we found that miR-26a level was down-regulated in LSCC tissues and cell lines, while CKS2 expression was increased. Cell proliferation, migration, invasion and the expression of MMP2 and MMP9 was suppressed by miR-26a overexpression, but enhanced by inhibition of miR-26a. Dual-luciferase reporter assay demonstrated that CKS2 is a direct target of miR-26a in AMC-HN-8 cells. Overexpression of miR-26a caused a significant reduction in CKS2 expression, and reinforced expression of CKS2 abolished the tumour-suppressive function of miR-26a. Moreover, miR-26a inhibited tumour growth in vivo. Taken together, miR-26a inhibited proliferation and tumourigenesis of LSCC via targeting CKS2 in vitro and in vivo.

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Section: Discussionsupporting

confidence: 87%

Section: Introductionmentioning

confidence: 99%

MicroRNA‐26a inhibits proliferation and tumorigenesis via targeting CKS2 in laryngeal squamous cell carcinoma

et al. 2018

Clin Exp Pharma Physio

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“…The serum miRNA profiles from samples taken both before and after tumor resections demonstrated an higher miR‐26 expression prior the oral squamous cell carcinoma surgical removal (Maclellan et al., ). However, other studies demonstrated that miR‐26 is downregulated and may exhibit tumor‐suppressive activity in other types of cancer, including esophageal squamous cancer (Li et al., ), besides promotes chemosensitivity to doxorubicin and promotes apoptosis of hepatocellular carcinoma cells (Jin et al., ).…”

Section: Discussionmentioning

confidence: 99%

Clinicopathological significance of miR‐26, miR‐107, miR‐125b, and miR‐203 in head and neck carcinomas

et al. 2018

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“…Increased expression of MYC can facilitate MYCBP translocation into the nucleus in the S phase of the cell cycle and influence proliferation, differentiation and apoptosis of cells . Recently published papers showed that MYCBP played an important role in lung cancer, gastric cancer, glioma, esophageal squamous cancer and acute myeloid leukaemia . However, it still remains unknown as to whether MYCBP plays a role in HCC.…”

Section: Introductionmentioning

confidence: 99%

EYA4 inhibits hepatocellular carcinoma by repressing MYCBP by dephosphorylating β‐catenin at Ser552

Zhu

Cai

et al. 2019

Cancer Science

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Hepatocellular carcinoma (HCC) is one of the most common malignancies and the fourth leading cause of cancer‐related death worldwide. Our previous study showed that EYA4 functioned by suppressing growth of HCC tumor cells, but its molecular mechanism is still not elucidated. Based on the results of gene microassay, EYA4 was inversely correlated with MYCBP and was verified in human HCC tissues by immunohistochemistry and western blot. Overexpressed and KO EYA4 in human HCC cell lines confirmed the negative correlation between EYA4 and MYCBP by qRT‐PCR and western blot. Transfected siRNA of MYCBP in EYA4 overexpressed cells and overexpressed MYCBP in EYA4 KO cells could efficiently rescue the proliferation and G2/M arrest effects of EYA4 on HCC cells. Mechanistically, armed with serine/threonine‐specific protein phosphatase activity, EYA4 reduced nuclear translocation of β‐catenin by dephosphorylating β‐catenin at Ser552, thereby suppressing the transcription of MYCBP which was induced by β‐catenin/LEF1 binding to the promoter of MYCBP. Clinically, HCC patients with highly expressed EYA4 and poorly expressed MYCBP had significantly longer disease‐free survival and overall survival than HCC patients with poorly expressed EYA4 and highly expressed MYCBP. In conclusion, EYA4 suppressed HCC tumor cell growth by repressing MYCBP by dephosphorylating β‐catenin S552. EYA4 combined with MYCBP could be potential prognostic biomarkers in HCC.

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miR-26a and miR-26b inhibit esophageal squamous cancer cell proliferation through suppression of c-MYC pathway

Cited by 73 publications

References 28 publications

MicroRNA‐26a inhibits proliferation and tumorigenesis via targeting CKS2 in laryngeal squamous cell carcinoma

MicroRNA‐26a inhibits proliferation and tumorigenesis via targeting CKS2 in laryngeal squamous cell carcinoma

Clinicopathological significance of miR‐26, miR‐107, miR‐125b, and miR‐203 in head and neck carcinomas

EYA4 inhibits hepatocellular carcinoma by repressing MYCBP by dephosphorylating β‐catenin at Ser552

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