miR‐204 is dysregulated in metastatic prostate cancer in vitro

Todorova, Krassimira; Metodiev, Metodi V.; Metodieva, Gergana; Zasheva, Diana; Mincheff, Milcho; Hayrabedyan, Soren

doi:10.1002/mc.22263

Cited by 24 publications

(19 citation statements)

References 70 publications

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“…The consensus sequence for TRA2β-binding (GAA) lies within the miR-204-binding site of BCL-2 3′-UTR, TRA2β antagonizes the effects of miR-204 and upregulates BCL-2 expression [54]. Such a mechanism is very interesting, partially because it can explain why miR-204 regulates expression of its targets with different efficiencies in the way depending on cell lines used [44]. Given that TRA2β mRNA expression is significantly upregulated in colon cancer [54] and prostate cancer tissues compared with paired normal tissues, it is highly possible that TRA2β plays an important role in carcinogenesis by blocking function of miR-204.…”

Section: Factors Regulating Expression and Function Of Mir-204mentioning

confidence: 99%

The dual regulatory role of miR-204 in cancer

Pan

2016

Tumor Biol.

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MicroRNAs (miRNAs) are a group of endogenous, small (about 22 nucleotides) non-coding RNAs which negatively regulate gene expressions. As one of them, miR-204 originates from the sixth intron of the transient receptor potential melastatin 3 (TRPM3) gene. Therefore, expression of miR-204 is under the control of the TRPM3 promoter and regulated by genetic and epigenetic mechanisms. miR-204 has been found to play the important roles in development of eyes and adipogenesis. Its pathological functions have been observed in a few diseases including pulmonary arterial hypertension, diabetes, and various types of cancers. It is believed that miR-204 acts as a tumor-suppressor via promoting apoptosis, conferring the resistance of cancer cells to chemotherapy, and suppressing the self-renewal of cancer stem cells (CSCs) and the epithelial to mesenchymal transition (EMT). Expression of miR-204 is repressed by its targets XRN1 and TRKB in prostate cancer and endometrial carcinoma, respectively; therefore, they establish an oncogenic feedback loops that play an important role promoting development of cancer. In this review, we summarize our current knowledge regarding miR-204, including its expression, regulation and biological functions, especially focusing our discussion on its role in tumor development and tumor progression.

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Section: Factors Regulating Expression and Function Of Mir-204mentioning

confidence: 99%

The dual regulatory role of miR-204 in cancer

Pan

2016

Tumor Biol.

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“…Dysregulation of miR-204 is a common feature in a number of cancers, such as breast cancer, acute myeloid leukemia, and prostate cancer (Butrym et al, 2015;Wang et al, 2015;Todorova et al, 2016). Although miR-204 has been found to be downregulated in GC tissues (Zhang et al, 2015a), its expression profile in serum samples and its potential for clinical use are unknown.…”

Section: Introductionmentioning

confidence: 99%

Reduced expression of serum miR-204 predicts poor prognosis of gastric cancer

Chen

Liu

et al. 2016

Genet. Mol. Res.

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ABSTRACT. Deregulation of microRNAs (miRNAs) is implicated in the initiation and progression of gastric cancer (GC). Previous studies have demonstrated that miR-204 was downregulated in GC tissues. However, its expression profile in serum samples and its potential for clinical value remain unknown. Real-time PCR was performed to evaluate the expression level of serum miR-204 in patients with GC. The association between serum miR-204 expression level and the clinical outcome of GC was then investigated. Our results showed that the expression of miR-204 in serum samples from GC patients was significantly lower than that in the healthy controls (P < 0.01). Serum miR-204 expression level of GC patients was significantly upregulated after receiving surgical resection (P < 0.01). In addition, serum miR-204 was associated with lymph node metastasis (P = 0.016), tumor differentiation (P = 0.001), and TNM stage (P = 0.005). GC patients with low serum miR-204 expression had shorter overall survival than those with high serum miR-204 expression (P = 0.004). Multivariate analysis revealed that serum miR-204 expression level was an independent risk factor for this malignant disease (HR = 3.629, 95%CI = 2.828-8.146, P = 0.015). In conclusion, our findings indicate that serum miR-204 may be employed as a novel biomarker for monitoring the treatment response and predicting the prognosis of GC.

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“…Previous studies had extensively confirmed that MicroRNAs played vital roles in tumor metastasis (9–11). Nevertheless, there are very few comprehensive reports on the prediction and diagnosis values of microRNAs in metastatic PCa (12).…”

Section: Introductionmentioning

confidence: 93%

Loss of miR-449a-caused PrLZ overexpression promotes prostate cancer metastasis

Chen

Liu

Chen

et al. 2017

International Journal of Oncology

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Distant metastasis is the worst prognostic factor for PCa patients. It has been reported that miR-449a enhances radiosensitivity of prostate cancer cells, but the function of miR449a in metastasis of prostate cancer is mainly unknown. In the present study, we strove to investigate the function and diagnostic value of miR-449a in metastasis of prostate cancer. qRT-PCR was used to quantify the expression of miR449a and PrLZ in PCa cell lines and tissues. We found that miR449a expression was decreased in PCa cell lines. Moreover, miR-449a was downregulated in PCa tissues, especially in primary lesion tissues of metastatic PCa patients. CCK8, FACS, Transwell and tube formation assay were performed to assess growth and metastasis of PCa cells in vitro. Lentivirus mediated miR-449a overexpression suppressed proliferation of LNcap and PC-3, and miR-449a also significantly inhibited invasion and angiogenesis ability of LNcap and PC-3. IHC showed that PrLZ was upregulated in PCa tissues. Luciferase assay and western blotting verified that miR-449a targeted PrLZ expression. Moreover, PrLZ shRNA also significantly suppressed proliferation and metastasis of LNcap and PC-3. In addition, western blotting revealed that miR-449a overexpression and PrLZ shRNA all remarkably inhibited the stemness features in LNcap and PC-3. Furthermore, BALB/c nude mouse subcutaneous xenograft model was uesd to verify the function of miR-449a and PrLZ. Our results showed that miR-449a and PrLZ shRNA significantly suppressed PC-3 tumorigenesis and metastasis in vivo. Our studies suggested that miR-449a decreased in malignant process of PCa and was accompanied by excess expression of PrLZ. The loss of miR-449a caused PrLZ overexpression regulated prostate cancer progression and metastasis via regulating the stemness features of prostate cancer cells. The diagnostic value of miR-449a as a distant metastasis predictor of PCa needs further investigation.

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miR‐204 is dysregulated in metastatic prostate cancer in vitro

Cited by 24 publications

References 70 publications

The dual regulatory role of miR-204 in cancer

The dual regulatory role of miR-204 in cancer

Reduced expression of serum miR-204 predicts poor prognosis of gastric cancer

Loss of miR-449a-caused PrLZ overexpression promotes prostate cancer metastasis

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