MiR-17-5p enhances pancreatic cancer proliferation by altering cell cycle profiles via disruption of RBL2/E2F4-repressing complexes

Zhu, Youwei; Gu, Jiangning; Liu, Ying; Peng, Chenghong; Shi, Minmin; Wang, Xuelong; Wei, Gang; Ge, Ouyang; Wang, Di; Zhang, Bosen; Wu, Jian; Zhong, Yiming; Shen, Baiyong; Chen, Hao

doi:10.1016/j.canlet.2017.09.044

Cited by 78 publications

(61 citation statements)

References 33 publications

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“…miR‐17‐5p was regarded as onco‐miR‐1, which is commonly regarded as the first identified oncogenic miRNA . Increased expression and oncogenic roles of miR‐17‐5p have been reported in breast cancer, pancreatic cancer, B‐cell lymphoma, liver cancer, and so on . In this study, we further demonstrated that via physically binding to miR‐17‐5p, PAX8‐AS1‐N up‐regulated miR‐17‐5p targets, such as PTEN, CDKN1A (p21), ZBTB4, which are critical tumor suppressors in many cancers.…”

Section: Discussionsupporting

confidence: 50%

“…[54][55][56][57] Increased expression and oncogenic roles of miR-17-5p have been reported in breast cancer, pancreatic cancer, B-cell lymphoma, liver cancer, and so on. 42,45,58,59 In this study, we further demonstrated that via physically binding to miR-17-5p, PAX8-AS1-N up-regulated miR-17-5p targets, such as PTEN, CDKN1A (p21), ZBTB4, which are critical tumor suppressors in many cancers. Through activating PAX8-AS1-N, baicalein up-regulated PTEN, CDKN1A, and ZBTB4.…”

Section: Discussionmentioning

confidence: 52%

“…miR-17-5p was frequently reported to function as an oncogenic miRNA in many cancers, including breast cancer. [42][43][44][45] To investigate whether PAX8-AS1-N genuinely binds to miR-17-5p, we carried out RNA pull down assays using in vitro transcribed biotin-labeled PAX8-AS1-N. As shown in Figure 6C, PAX8-AS1-N specifically bound to miR-17-5p, but not miR-200b which did not have predicted binding site on PAX8-AS1-N. The well-known tumor suppressors PTEN, CNDK1A (p21), and ZBTB4 were reported to be critical targets of miR-17-5p.…”

Section: Cdkn1a and Zbtb4 Expression Via Interacting With Mir-17-5pmentioning

confidence: 99%

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Baicalein inhibits breast cancer growth via activating a novel isoform of the long noncoding RNA PAX8‐AS1‐N

Cao

Tang

et al. 2018

J of Cellular Biochemistry

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Baicalein, a natural flavonoid, has fascinating anti-cancer properties in breast cancer. Long noncoding RNAs (lncRNAs), a class of transcripts with no protein-coding potential, also exhibit critical roles in breast cancer. However, the molecular mechanisms mediating the anti-cancer properties of baicalein and whether lncRNAs are involved in the anti-cancer effects are still unclear. In this study, we identified a novel isoform of lncRNA PAX8-AS1 (PAX8-AS1-N), which is activated by baicalein in a dose- and time-dependent manner. Functional assays showed that PAX8-AS1-N reduced cell viability, inhibited cell-cycle progression, and induced apoptosis of breast cancer cells in vitro. Depletion of PAX8-AS1-N promoted breast xenograft tumor growth in vivo. Furthermore, depletion of PAX8-AS1-N attenuated the suppressive roles of baicalein on cell viability, the apoptosis induced by baicalein, and also the suppressive roles of baicalein on tumor growth in vivo. Mechanistically, PAX8-AS1-N bound to miR-17-5p, and up-regulated miR-17-5p targets, such as PTEN, CDKN1A, and ZBTB4. In addition, PAX8-AS1-N was down-regulated in breast cancer and reduced expression of PAX8-AS1-N indicated poor survival of breast cancer patients. In conclusion, our results demonstrated that PAX8-AS1-N activation mediated the anti-cancer effects of baicalein via regulating miR-17-5p, and suggested that baicalein and enhancing PAX8-AS1-N would be potential therapeutic strategies against breast cancer.

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Section: Discussionsupporting

confidence: 50%

Section: Discussionmentioning

confidence: 52%

Section: Cdkn1a and Zbtb4 Expression Via Interacting With Mir-17-5pmentioning

confidence: 99%

See 1 more Smart Citation

Baicalein inhibits breast cancer growth via activating a novel isoform of the long noncoding RNA PAX8‐AS1‐N

Cao

Tang

et al. 2018

J of Cellular Biochemistry

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“…Moreover, downregulation of miR‐17 reduces chemoresistance and represses EMT in a death effector domain‐containing DNA‐binding protein‐dependent manner in gastric cancer cells . MiR‐17‐5p is also reported to promote cancer cell proliferation via changing cell cycle profiles by dysregulating the retinoblastoma‐like protein 2/E2F4‐repressing complexes . More importantly, miR‐17‐5p has also been reported as an oncological gene in prostate cancer as well.…”

Section: Discussionmentioning

confidence: 99%

Circ‐MTO1 correlates with favorable prognosis and inhibits cell proliferation, invasion as well as miR‐17‐5p expression in prostate cancer

Guo

2019

Clinical Laboratory Analysis

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Background This study aimed to investigate circular RNA‐mitochondrial tRNA translation optimization 1 (circ‐MTO1) expression in tumor tissue and its correlation with clinical characteristics and survival profiles, as well as its effect on cancer cell functions in prostate cancer. Methods A total of 298 primary prostate cancer patients were included. Reverse transcription‐quantitative polymerase chain reaction was conducted to evaluate circ‐MTO1 expression in tumor tissue and paired adjacent tissue. Disease‐free survival (DFS) and overall survival (OS) were recorded. In in vitro experiment, prostate cancer cells were transfected with circ‐MTO1 over‐expression and negative‐control over‐expression plasmids. Then cell proliferation, cell invasion and miR‐630 as well as miR‐17‐5p expressions in prostate cancer cells were detected. Results Circular RNA‐mitochondrial tRNA translation optimization 1 expression was downregulated in tumor tissue compared with paired adjacent tissue (P < .001) in patients with prostate cancer. Circ‐MTO1 high expression in tumor tissue was correlated with decreased pathological T stage (P = .001) as well as lower pathological N stage (P = .020). As for survival profiles, the DFS (P = .006) and OS (P = .018) were both longer in patients who had circ‐MTO1 high expression compared with patients who had circ‐MTO1 low expression. In addition, circ‐MTO1 high expression independently predicted favorable DFS and OS. Besides, further in vitro experiments illustrated that circ‐MTO1 inhibited proliferation (P < .05) and invasion (P < .05) as well as downregulated miR‐17‐5p expression in prostate cancer cells (P < .05). Conclusion Circ‐MTO1 correlates with decreased pathological T/N stage and favorable survival profiles, and it also inhibits cell proliferation, invasion as well as miR‐17‐5p expression in prostate cancer.

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“…All differentially expressed miRNAs are listed according to tumor type in Supporting Table 4. [24][25][26][27][28][29][30][31][32][33][34][35][36][37] Investigation of these miRNAs within published data indicates their role in oncogenesis. 2A) We performed pathway analysis to determine the clinical significance and biologic functions of the differentially expressed miRNAs for each cancer type.…”

Section: Mirna Analysismentioning

confidence: 99%

Pan‐cancer clinical and molecular analysis of racial disparities

Lara

Wang

Asare

et al. 2019

Cancer

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Background Racial disparities in cancer outcomes are increasingly recognized, but comprehensive analyses, including molecular studies, are limited. The objective of the current study was to perform a pan‐cancer clinical and epigenetic molecular analysis of outcomes in African American (AA) and European American (EA) patients. Methods Cross‐platform analyses using cancer databases (the Surveillance, Epidemiology, and End Results program database and the National Cancer Data Base) and a molecular database (The Cancer Genome Ancestry Atlas) were performed to evaluate clinical and epigenetic molecular differences between AA and EA patients based on genetic ancestry. Results In the primary pan‐cancer survival analysis using the Surveillance, Epidemiology, and End Results database (2,045,839 patients; 87.5% EA and 12.5% AA), AA patients had higher mortality rates for 28 of 42 cancer types analyzed (hazard ratio, >1.0). AAs continued to have higher mortality in 13 cancer types after adjustment for socioeconomic variables using the National Cancer Database (5,150,023 patients; 11.6% AA and 88.4% EA). Then, molecular features of 5,283 tumors were analyzed in patients who had genetic ancestry data available (87.2% EA and 12.8% AA). Genes were identified with altered DNA methylation along with increased microRNA expression levels unique to AA patients that are associated with cancer drug resistance. Increased miRNAs (miR‐15a, miR‐17, miR‐130‐3p, miR‐181a) were noted in common among AAs with breast, kidney, thyroid, or prostate carcinomas. Conclusions The current results identified epigenetic features in AA patients who have cancer that may contribute to higher mortality rates compared with EA patients who have cancer. Therefore, a focus on molecular signatures unique to AAs may identify actionable molecular abnormalities.

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MiR-17-5p enhances pancreatic cancer proliferation by altering cell cycle profiles via disruption of RBL2/E2F4-repressing complexes

Cited by 78 publications

References 33 publications

Baicalein inhibits breast cancer growth via activating a novel isoform of the long noncoding RNA PAX8‐AS1‐N

Baicalein inhibits breast cancer growth via activating a novel isoform of the long noncoding RNA PAX8‐AS1‐N

Circ‐MTO1 correlates with favorable prognosis and inhibits cell proliferation, invasion as well as miR‐17‐5p expression in prostate cancer

Pan‐cancer clinical and molecular analysis of racial disparities

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