Biological function and mechanism of miR-33a in prostate cancer survival and metastasis: via downregulating Engrailed-2

Li, Q.; Lu, Shuaibing; Li, X.; Hou, Guoqing; Liang, Yan; Zhang, W.; Qiao, Baohua

doi:10.1007/s12094-016-1564-3

Cited by 10 publications

(11 citation statements)

References 27 publications

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“…Even PSA which has become a widely used marker for early diagnose of PC showed no clear correlation with the clinical stages of PC. This result further confirmed EN2 is more suitable as a diagnose target than PSA with better veracity and sensitivity, which consistent with the previous studies [20,27].…”

Section: Discussionsupporting

confidence: 92%

“…The EN2 protein we used as immunogen has been confirmed to be the main functional structural domain of EN2's exocrine and internalization [18,19]. Some studies also showed this part of EN2 is available to produce detectable antibodies for PC patients' urine test [20,21]. The monoclonal antibody against this part of EN2 could present different staining pattern in BPH and PC.…”

Section: Discussionmentioning

confidence: 94%

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Altered staining patterns and expression level of Engrailed-2 in Benign prostatic hyperplasia and Prostate Cancer predict Prostatic disease progression

Shi

Sa³

et al. 2019

Preprint

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Background: Prostate cancer (PC) as a kind of malignant tumor, causes the most death of cancer among males. Successful curing of PC greatly relies on its diagnose in the early stage. Engrailed-2 (EN2), which has been confirmed being existed in the high level in the urine of PC patients, has not been reported as a histochemical diagnostic biomarker of PC. In this study, we analyzed the EN2 expression level and staining patterns in PC and benign prostatic hyperplasia (BPH) samples for seeing the change of EN2 in PC early stage. Methods: EN2 monoclonal antibody was generated and the specificity of this antibody was validated with different maneuvers. Endogenic and exogenous of EN2 in three PC cell lines (LNCap, PC3, and DU145) was detected by immunofluorescence. The expression level and staining patterns of EN2 in 25 of PC and 25 of BPH tissues were detected by immunohistochemistry. RT-PCR was done for further conforming whether EN2 is overexpressed in PC and BPH tissues. Finally, a relationship of EN2 expression and PC occurrence was obtained by case analysis of PC. Results: The results of WB and immunofluorescence showed the monoclonal antibody of EN2 we made could specifically bind endogenic and ectogenic EN2 protein in three different PC cell lines. Results of immunofluorescence showed the endogenic EN2 was generally expressed in the cytoplasm and ectogenic EN2 has mostly existed in the nucleus. Immunohistochemical staining of EN2 in PC was extremely higher than in BPH confirmed by RT-PCR. The staining areas were mostly nucleus and cytoplasm in BPH tissues but cytomembrane in PC tissues. The expression level of EN2 was positively correlated with the PC clinical stage. Conclusion: The EN2 monoclonal antibody we made could distinguish BPH and PC by immunohistochemistry. The expression level and tissue distribution pattern of EN2 can help with the determination of PC’s progression.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 94%

Altered staining patterns and expression level of Engrailed-2 in Benign prostatic hyperplasia and Prostate Cancer predict Prostatic disease progression

Shi

Sa³

et al. 2019

Preprint

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“…miRNAs are identified as critical regulators of cancer growth and metastasis (24,25). Among numerous miRNAs, miR-33a has been confirmed as a critical tumor-suppressive miRNA and a prognostic marker of human cancers including NSCLC (9,26) and pancreatic cancer (16), while, miR-33a exerts an oncogenic role in prostate cancer (17) and glioblastoma (19). Here, our data indicated that overexpression of miR-33a was common in glioma tissues.…”

Section: Discussionmentioning

confidence: 55%

“…Previous research indicates that miR-33a expression is inhibited in various cancer types including NSCLC, gallbladder cancer, hepatocellular carcinoma (HCC), breast cancer, melanoma and pancreatic cancer (9)(10)(11)(12)(13)(14)(15)(16). However, overexpression of miR-33a has been reported in prostate cancer (17). Furthermore, miR-33a was found to contribute to osteosarcoma chemoresistant by reducing cisplatin-induced cell apoptosis (18).…”

Section: Introductionmentioning

confidence: 99%

Suppression of SIRT6 by miR-33a facilitates tumor growth of glioma through apoptosis and oxidative stress resistance

Chang

Lin²,

et al. 2017

Oncology Reports

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microRNA-33a (miR-33a) belongs to the miR-33 family that is implicated in the progression of various types of cancers. Aberrant expression of miR-33a has been detected in several human cancers, and has been shown to regulate the migration and invasion as well as proliferation and apoptosis of tumor cells. However, the clinical significance and precise mechanisms underlying the dysfunction of miR-33a in glioma have not been well investigated in previous studies. In this study, overexpression of miR-33a was observed in clinical glioma specimens and cell lines. Clinicopathological detection revealed that miR-33a highly expressing patients showed large tumor sized and advanced World Health Organization (WHO) grade as well as reduced overall survival. Furthermore, the results of in vitro experiments confirmed that loss of miR-33a resulted in reduced proliferation and enhanced apoptosis in U251 cells, while miR-33a restoration showed opposite effects in U87 cells. Further studies indicated that miR-33a knockdown restrained tumor growth of glioma in vivo. miR-33a negatively regulated the expression of sirtuin 6 (SIRT6) at both mRNA and protein levels via targeting the 3'UTR of SIRT6 mRNA. SIRT6 was underexpressed and inversely correlated with miR-33a expression in the glioma tissues. Mechanistically, SIRT6 overexpression increased the levels of lactate dehydrogenase (LDH) and reactive oxygen species (ROS) while it reduced cell survival under H2O2 treatment. In addition, SIRT6 restoration led to apoptosis with alterative expression of Bax, Bcl-2, cleaved caspase-8, and inhibition of Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway in glioma. Thus, our studies demonstrated that the deregulation of miR-33a may promote tumor development in human glioma by regulating the expression of its target gene, SIRT6.

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“…7A). Li et al (107) have demonstrated that miR-33a is a tumor suppressor in PC, and high levels of miR-33a downregulate its target gene engrailed homeobox 2, thereby suppressing the proliferation, migration and invasion of PC cells (Fig. 7B).…”

Section: Male and Female Cancer Prostate Cancer (Pc)mentioning

confidence: 96%

Role of microRNA‑33a in malignant cells (Review)

et al. 2020

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Cancer causes most of the mortality and morbidity worldwide, with a significant increase in incidence during recent years. MicroRNAs (miRNAs/miRs) are non-coding small RNAs capable of regulating gene expression. They regulate crucial cellular processes, including proliferation, differentiation, metastasis and apoptosis. Therefore, abnormal miRNA expression is associated with multiple diseases, including cancer. There are two types of cancer-associated miRNAs, oncogenic and tumor suppressor miRNAs, depending on their roles and expression patterns in cancer. Accordingly, miRNAs are considered to be targets for cancer prevention and treatment. miR-33a controls cellular cholesterol uptake and synthesis, which are both closely associated with carcinogenesis. The present review thoroughly describes the roles of miR-33a in more than a dozen types of cancer and the underlying mechanisms. Accordingly, the present review may serve as a guide for researchers studying the involvement of miR-33a in diverse cancer settings. Contents 1. Introduction 2. miR-33a and its role in cancer 3. Discussion 4. Conclusions

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Biological function and mechanism of miR-33a in prostate cancer survival and metastasis: via downregulating Engrailed-2

Abstract: Our data suggest that the functional interaction of miR-33a and EN-2 is involved in tumorigenesis of prostate cancer. Also in this process EN-2 serves as a negative responder for miR-33a.

Cited by 10 publications

References 27 publications

Altered staining patterns and expression level of Engrailed-2 in Benign prostatic hyperplasia and Prostate Cancer predict Prostatic disease progression

Altered staining patterns and expression level of Engrailed-2 in Benign prostatic hyperplasia and Prostate Cancer predict Prostatic disease progression

Suppression of SIRT6 by miR-33a facilitates tumor growth of glioma through apoptosis and oxidative stress resistance

Role of microRNA‑33a in malignant cells (Review)

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