miR-326 functions as a tumor suppressor in human prostatic carcinoma by targeting Mucin1

Liu, Xuan; Li, Zhaolun; Men, Qun-Li; Li, Yongwei; Li, Hechen; Chong, Tie

doi:10.1016/j.biopha.2018.09.053

Cited by 36 publications

(30 citation statements)

References 33 publications

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“…The major finding of the current study was that miR-326 inhibited proliferation and invasion of breast cancer cells through targeting SOX12, revealing a novel epigenetic mechanism of how miR-326 played a tumor suppressive role in breast cancer. Growing evidence has shown that miR-326 functioned as a tumor suppressor in multiple types of malignant tumors [11][12][13][14][15][16][17]. Although a study showed that miR-326 implicate in chemotherapy resistance of breast cancer through regulating expression of multidrug resistance-associated protein 1 [28], its functional role and underlying mechanism in breast cancer remained largely unknown.…”

Section: Discussionmentioning

confidence: 99%

“…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%

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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: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Functional analyses of microRNA-326 in breast cancer development

Shen

Zhang

et al. 2019

Bioscience Reports

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“…As our experiment revealed, miR-326 was down-regulated in BC tissues or cells, while the overexpression of miR-326 resulted in inhibition of proliferation, invasion, and angiogenesis of BC cells. Likewise, previous evidence has shown that miR-326 may act as an anti-tumor miR in the occurrence and development of human prostatic carcinoma (10). Consistent with our findings, miR-326 was down-regulated in the tissues and cell lines of human BC, and the overexpressed miR-326 has been showed to inhibit the cell proliferation, migration, and invasion of BC (11).…”

Section: Discussionsupporting

confidence: 92%

“…Prior to the current investigation, a targeting relationship between miR-326 and circRNA hsa_circ_0000517 (hsa_circRPPH1_015) was assessed by using CircInteractome database (https://circinteractome.nia.nih.gov/index.html). miR-326 highlights itself as an antioncomiR in pro-static carcinoma by negatively regulates Mucin1 (10). Additionally, miR-326 has been noted to harbor tumor-suppressive property in BC (11).…”

Section: Introductionmentioning

confidence: 99%

A Novel Circular RNA hsa_circRPPH1_015 Exerts an Oncogenic Role in Breast Cancer by Impairing miRNA-326-Mediated ELK1 Inhibition

Zhao

et al. 2020

Front. Oncol.

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Background: Breast cancer (BC) represents a heterogeneous disease with distinct subtypes and high tumor metastatic potentials. Recent researchers identify the implication of circular RNAs (circRNAs) in the initiation of BC. Herein, we uncover a novel circRNA hsa_circRPPH1_015 as a tumor promoter in BC. Methods: A total of 86 paired cancerous and non-cancerous tissues were surgically resected and collected from BC patients. Cell proliferation, colony formation, and cell invasion were examined by Edu staining, clone formation assays, propidium iodide (PI)-labeled flow cytometry, and Transwell invasion assays. PCNA, Ki67, MMP-2, MMP-9, Cyclin D1, and CDK4 expression was assayed using Western blot analysis. RNA pull-down, dual-luciferase reporter gene assay, and RNA binding protein immunoprecipitation (RIP) assay were performed to investigate the relationships among hsa_circRPPH1_015, microRNA-326 (miR-326), and ELK1. The tumor growth of human BC MCF-7 cells in vivo was evaluated in nude mice by subcutaneous xenografts of MCF-7 cells. Results: hsa_circRPPH1_015 expression was upregulated in BC tissues. Knockdown of hsa_circRPPH1_015 restrained the aggressive behavior of MCF-7. hsa_circRPPH1_015 could bind to miRNA-326 that negatively regulates ELK1. Elevation of miRNA-326 expression resulted in inhibition of cell proliferation, colony formation, and cell invasion of MCF-7. Disturbance of miRNA-326 or overexpression of ELK1 restored the proliferation and aggressiveness in hsa_circRPPH1_015-depleted MCF-7 cells. Tumor growth of MCF-7 cells in vivo was reduced in nude mice lack of endogenous hsa_circRPPH1_015 expression. Conclusion: Overall, the present study demonstrates that hsa_circRPPH1_015 was an oncogene and unfavorable prognostic factor in BC, providing an exquisite therapeutic target for BC.

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“…In current study, miR-326 was recognized as the shared miRNA between SNHG12 and E2F1. Also, here we discovered marked downregulation of miR-326 expression in OSCC tissues and cell lines, which was consistent with its level in many other cancer types, such as lung cancer (Wang et al, 2016), osteosarcoma (Cao, Wang, & Wang, 2016), prostatic carcinoma (Liang et al, 2018), and so on. Moreover, miR-326 sponged by lncRNAs has also been unveiled in several cancers, for instance, hepatocellular carcinoma (Wei et al, 2019).…”

Section: Discussionsupporting

confidence: 87%

SNHG12/miR‐326/E2F1 feedback loop facilitates the progression of oral squamous cell carcinoma

et al. 2020

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Oral squamous cell carcinoma (OSCC) is a prevalent cancer affecting the head and neck region (Bozec, Peyrade, Fischel, & Milano, 2009). It alarmingly represents approximately 3% of all malignant cases (Jin et al., 2016). OSCC is characterized by high morbidity and mortality, with more than 300,000 new OSCC cases and over 140,000 deaths of OSCC patients every year (Chi, Day, & Neville, 2015; Sasahira & Kirita, 2018). Although surgery combined with radiotherapy, neoadjuvant chemotherapy, and targeted therapy has greatly improved the treatment of OSCC, the overall 5-year survival rate of OSCC patients has remained to be around 50% (

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miR-326 functions as a tumor suppressor in human prostatic carcinoma by targeting Mucin1

Cited by 36 publications

References 33 publications

Functional analyses of microRNA-326 in breast cancer development

Functional analyses of microRNA-326 in breast cancer development

A Novel Circular RNA hsa_circRPPH1_015 Exerts an Oncogenic Role in Breast Cancer by Impairing miRNA-326-Mediated ELK1 Inhibition

SNHG12/miR‐326/E2F1 feedback loop facilitates the progression of oral squamous cell carcinoma

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