Up-regulation of microRNA in bladder tumor tissue is not common

Wang, Gang; Zhang, Honghe; He, Honghua; Tong, Wenjuan; Wang, Bin; Liao, Guodong; Chen, Zhao-Dian; Du, Caigan

doi:10.1007/s11255-009-9584-3

Cited by 69 publications

(45 citation statements)

References 35 publications

(38 reference statements)

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“…Although non-differential expression of miR-30c was observed in cervical cancer cell lines (22) and nasopharyngeal carcinoma tissues (23) compared to the normal controls, most studies have suggested that miR-30c acts as a tumor suppressor and is weakly expressed in cancers such as breast cancer (24), bladder cancer (14), medulloblastoma (15) and clear-cell renal cell carcinoma (25), depending on the tissue context. In this report, we demonstrated the antitumor role of miR-30c in endometrial cancer cells.…”

Section: Discussionmentioning

confidence: 99%

“…Total RNA was isolated using TRIzol reagent (Invitrogen) and then both miRNA and mRNA were reversetranscribed to cDNA with the Reverse Transcriptase M-MLV kit (Takara, China). The stem-loop RT primer for miR-30c was 5'-GTCGTATCCAGTGCAGGGTCCGAGTATTCGC ACTGGATACGACGCTGA-3' (14). U6 small nuclear RNA was used as an internal control.…”

Section: Methodsmentioning

confidence: 99%

“…Particularly, the loss of expression of miR-30c occurs in many types of malignancies, including endometrial cancer (14)(15)(16). miR-30c has been proposed to impact human pulmonary endothelial cells through targeting the 3'-UTR of plasminogen activator inhibitor-1 (PAI1) (17).…”

Section: Microrna-30c Negatively Regulates Endometrial Cancer Cells Bmentioning

confidence: 99%

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microRNA-30c negatively regulates endometrial cancer cells by targeting metastasis-associated gene-1

Zhou

Xu²,

Xun³

et al. 2011

Oncol Rep

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Abstract.It is well known that microRNAs (miRNAs) play important roles in cancer development by targeting oncogenes or tumor-suppressor genes. However, little is known regarding the mechanisms of miR-30c action in endometrial cancer. In this study, we aimed to determine whether miR-30c targets metastasis-associated gene-1 (MTA1) and acts as a tumor suppressor in endometrial cancer cell lines Ishikawa (estrogen receptor-positive, ER + ) and HEC-1-B (ER -) by down-regulating MTA1. As a result, in both Ishikawa and HEC-1-B cells, realtime PCR demonstrated that overexpression of miR-30c led to the down-regulation of MTA1 mRNA (P<0.05), while Western blotting confirmed the reduced expression levels of MTA1 protein (P<0.01). A dual-luciferase reporter assay demonstrated that miR-30c was directly bound to the 3'-untranslated regions of MTA1. Then we studied the biological mechanisms of endometrial cancer cells transfected with the Pre-miR-30c plasmid. MTT assay and growth curves revealed that miR-30c inhibits both Ishikawa and HEC-1-B cell proliferation. However, we did not see obvious differences in rates of apoptosis between miR30c-overexpressing and the negative control cells. Then using wound-healing and Matrigel invasion assays, we found that the migratory and invasive abilities of cells transfected with the Pre-miR-30c plasmid were significantly suppressed compared with the control cells (P<0.01). Overall, our study, for the first time, showed that MTA1 is negatively regulated by miR-30c and that overexpression of miR-30c inhibits the proliferative, migratory and invasive abilities of endometrial cancer cells. These results suggest that miR-30c acts as a tumor suppressor and negatively regulates endometrial cancer cells by targeting MTA1. IntroductionEndometrial carcinoma is a common worldwide gynecologic malignancy. Two different clinicopathological subtypes of endometrial cancer are recognized: one is estrogen-related type 1 (endometroid), and the other is non-estrogen-related type 2 (non-endometroid such as papillary serous and clear cell) (1). Although various endocrine, genetic and external factors, such as unopposed estrogen exposure, complex hyperplasia with atypia, and treatment with tamoxifen during breast cancer therapy, may contribute to its initiation and progression, the etiology of endometrial carcinoma remains not fully understood (2). The primary and most effective treatment for patients with localized disease is still hysterectomy and bilateral salpingo-oophorectomy (3). Although adjuvant radiotherapy and chemotherapy may reduce local recurrence and systemic metastases, the associated toxicity and morbidity are significant (4). Thus, the search for novel molecular targets as therapeutic agents through an increased understanding of the molecular mechanisms of endometrial tumorigenesis is in urgent need. microRNAs (miRNAs) are a class of conserved short (19-25 nt) RNAs that regulate gene expression through basepairing with the 3'-untranslated regions (3'-UTR) of target mRNAs (5) and play an importa...

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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microRNA-30c negatively regulates endometrial cancer cells by targeting metastasis-associated gene-1

Zhou

Xu²,

Xun³

et al. 2011

Oncol Rep

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“…The decrease in expression of 4 miRNAs is common for all bladder tumors regardless of cancer stage or tumor differentiation. miR-26 may therefore be a significant marker in bladder cancer (20). Maillot et al observed that E2-repressed miR-26a and miR181a regulated numerous genes associated with cell growth and proliferation through estrogen receptors and transcription factors.…”

Section: Mir-26 and Tumors: Down-and Up-regulationmentioning

confidence: 99%

The role of miR-26 in tumors and normal tissues (Review)

Gao

Liu

2011

Oncology Letters

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“…Therefore, by targeting antiapoptotic gene (Cdc42,p85a,Mcl1 and Tcl1) and enhancing the inhibiting of tumor transcription, miR-29 chould inhibits the tumor growth effectively . In several researches, the genetic screening showed that the expression of miR-29 a/c in bladder cancer was down-regulated (Dyrskjot et al, 2009;Friedman et al, 2009;Wang et al, 2010). Baffa R et al showed that the expression of miR-29a/b was up-regulated in paired primary and metastatic cancers.…”

Section: Introductionmentioning

confidence: 99%

Exosome-derived microRNA-29c Induces Apoptosis of BIU-87 Cells by Down Regulating BCL-2 and MCL-1

Xu¹,

Wu²,

Fan³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Asian Pac J Cancer Prev, 15 (8), 3471-3476 IntroductionThe incidence of bladder carcinoma is in the first in Chinese urological tumor, which includes the 70% non invasive cancer and 30% invasive cancer. The patients accompanied with systemic metastasis have poor prognosis and a lifetime risk of recurrence.Tumor-derived exosomes had been regarded as a good carrier of anti-tumor therapy for its advantages of tumor specific antigen recognition, easy to obtain. For example, exosomes from tumor cells treated by heat shock or genetic modification were associated with ODN-CpG adjuvants to deal with the tumor bearing mice, showing that it enhanced the antitumor activity of the secretion of exosomes (Chaput et al., 2004). Researches on exosomesderived miRNA indicated that it could be used as a new

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Up-regulation of microRNA in bladder tumor tissue is not common

Cited by 69 publications

References 35 publications

microRNA-30c negatively regulates endometrial cancer cells by targeting metastasis-associated gene-1

microRNA-30c negatively regulates endometrial cancer cells by targeting metastasis-associated gene-1

The role of miR-26 in tumors and normal tissues (Review)

Exosome-derived microRNA-29c Induces Apoptosis of BIU-87 Cells by Down Regulating BCL-2 and MCL-1

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