miR-326 Inhibits Gastric Cancer Cell Growth Through Downregulating NOB1

Ji, Sheqing; Zhang, Bin; Kong, Yali; Ma, Fei; Hua, Yawei

doi:10.3727/096504016x14759582767486

Cited by 69 publications

(72 citation statements)

References 28 publications

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“…MicroRNA-326 (miR-326) was reported to be down-regulated and function as tumor suppressor in multiple cancers, including lung cancer [11], hepatocellular carcinoma [12], prostatic carcinoma [13], gastric cancer [14], osteosarcoma [15], glioblastoma [16] and nasopharyngeal carcinoma [17]. However, the expression pattern, possible functions and underlying mechanisms of miR-326 are yet to be described in breast cancer.…”

Section: Introductionmentioning

confidence: 99%

Functional analyses of microRNA-326 in breast cancer development

Shen

Zhang

et al. 2019

Bioscience Reports

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MicroRNA-326 (miR-326) was reported to be dysregulated and involved in the progression of multiple cancers. However, the clinical significance, biological role and underlying mechanism of miR-326 in the carcinogenesis of breast cancer are still unclear. In the present study, we showed that miR-326 was down-regulated in human breast cancer tissues and cell lines. Our results also revealed that miR-326 overexpression significantly suppressed breast cancer cell proliferation, migration and invasion, and induced cell cycle arrest at G1/G0 phase. Furthermore, Sex determining region Y-box (SOX) protein 12 (SOX12), a known oncogene, was identified as a direct target of miR-326 by luciferase reporter assay. Moreover, miR-326 expression was inversely correlated with SOX12 mRNA expression levels in human breast cancer specimens. Overexpression of SOX12 partially rescued the inhibitory effect on cell proliferation, migration and invasion in breast cancer cells caused by miR-326 overexpression. These findings suggested that miR-326 might play a suppressive role in breast cancer, at least in part, by targeting SOX12, rendering miR-326 a promising therapeutic target for breast cancer.

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Section: Introductionmentioning

confidence: 99%

Functional analyses of microRNA-326 in breast cancer development

Shen

Zhang

et al. 2019

Bioscience Reports

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“…They directly bind to the 3' untranslated region (UTR) of their target mRNA, and cause translation repression or mRNA degradation; thus, they are important regulators of gene expression (9,10). Various miRNA have been demonstrated to be involved in a variety of cellular biological processes, including cell proliferation, differentiation, survival, migration and invasion (8,(11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑302 inhibits cell migration and invasion in cervical cancer by targeting DCUN1D1

Jiang

Hou

et al. 2018

Exp Ther Med

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Abstract. MicroRNA serve crucial roles in a variety of human cancer types. The miR-302-367 cluster has been reported to suppress the proliferation of cervical carcinoma cells through the novel target AKT1; however, the molecular mechanism of miR-302 in cervical cancer metastasis remains unclear. The present study aimed to investigate the clinical significance of miR-302-3p expression in cervical cancer, and to examine the regulatory mechanism of miR-302-3p in the malignant phenotypes of cervical cancer cells. The present data indicated that miR-302-3p was significantly downregulated in cervical cancer tissues compared with the level in adjacent non-tumor tissues, and low expression of miR-302-3p was significantly associated with node metastasis, advanced clinical stage, and poor prognosis in patients with cervical cancer. Restoration of miR-302-3p expression caused a significant reduction in cervical cancer cell migration and invasion. Defective in cullin neddylation 1 domain containing 1 (DCUN1D1) was identified as a novel target gene of miR-302-3p, and miR-302-3p negatively regulated the mRNA and protein expression of DCUN1D1 in cervical cancer HeLa cells. Additionally, overexpression of DCUN1D1 rescued the effects of miR-302-3p on the migration and invasion of cervical cancer cells. Furthermore, DCUN1D1 was upregulated in cervical cancer tissues compared with the levels in adjacent tissues, and its high expression was associated with node metastasis, advanced clinical stage, and shorter survival time in patients with cervical cancer. Notably, a negative correlation between miR-302-3p and DCUN1D1 expression in cervical cancer tissues was observed. Taken together, the present study suggests that miR-302-3p serves a suppressive role in cervical cancer metastasis, partly at least, via directly targeting DCUN1D1. Therefore, miR-302-3p/DCUN1D1 may be a potential therapeutic target for cervical cancer treatment.

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“…Cao et al (38) found that miR-326 overexpression inhibited the growth and metastasis of osteosarcoma cells. In addition, studies reported that the enforced expression of miR-326 suppressed gastric cancer (gC) cell growth and metastasis and induced gC cell g2/M arrest (39,41). Furthermore, studies revealed that miR-326 served as a tumour-suppressor in glioma by inhibiting cell proliferation, colony formation and metabolic activity and inducing cell apoptosis (42,43).…”

Section: Discussionmentioning

confidence: 99%

“…Several miR-326 targets, including Bcl-2 (38) in osteosarcoma, FSCN1 (39) and NOB1 (41) in gastric cancer, SMO (47) and PKM2 (43) in glioma and CCND1 (25), phox2a (44), SP1 (45) and ADAM17 (46) in lung cancer, have been identified. In the present study, KRAS was validated as a novel target of miR-326.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-326 inhibits melanoma progression by targeting KRAS and suppressing the AKT and ERK signalling pathways

Kang

Zhang

et al. 2017

Oncol Rep

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Abstract. Melanoma is the seventh most common malignancy in females and the fifth most common cancer in males worldwide. An increasing number of studies have reported that microRNA (miRNA) dysregulation is frequently observed in various types of human cancers, including melanoma. Abnormally expressed miRNAs play an important role in melanoma formation and progression by serving as potential biomarkers and therapeutic targets. Recently, miRNA-326 (miR-326) has been reported to be differentially expressed in various types of tissues and play important roles in tumourigenesis and tumour development. However, the expression levels, biological roles and underlying mechanisms of miR-326 in melanoma remain unknown. In the present study, we demonstrated that miR-326 was significantly downregulated in melanoma tissues and cell lines. Functional assays revealed that the enforced expression of miR-326 suppressed melanoma cell proliferation and invasion and increased cell apoptosis in vitro. Using bioinformatic analysis, Kirsten rat sarcoma viral oncogene homolog (KRAS) was predicted as a potential target of miR-326. Luciferase reporter assay confirmed that miR-326 could directly target the 3'-untranslated region of KRAS. In addition, reverse transcription-quantitative polymerase chain reaction and western blot analysis revealed that miR-326 upregulation decreased the KRAS expression in melanoma cells at both the mRNA and protein level. Furthermore, KRAS was upregulated in melanoma tissues and inversely correlated with miR-326 expression. In addition, the KRAS knockdown phenocopied the tumour-suppressing effects of miR-326 overexpression on melanoma cells. The restoration of the expression of KRAS markedly reversed the antitumour effects induced by miR-326 overexpression in melanoma cells. Further experiments indicated that miR-326 inactivated the AKT and ERK signalling pathways in melanoma. Collectively, these results revealed that miR-326 serves as a tumour suppressor in melanoma by targeting KRAS and regulating the AKT and ERK signalling pathways, indicating that miR-326 may be a promising therapeutic target for melanoma patients.

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miR-326 Inhibits Gastric Cancer Cell Growth Through Downregulating NOB1

Cited by 69 publications

References 28 publications

Functional analyses of microRNA-326 in breast cancer development

Functional analyses of microRNA-326 in breast cancer development

MicroRNA‑302 inhibits cell migration and invasion in cervical cancer by targeting DCUN1D1

MicroRNA-326 inhibits melanoma progression by targeting KRAS and suppressing the AKT and ERK signalling pathways

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