Novel molecular targets regulated by tumor suppressors microRNA-1 and microRNA-133a in bladder cancer

Yamasaki, Takahiro; Yoshino, Hirofumi; Enokida, Hideki; Hidaka, Hideo; Chiyomaru, Takeshi; Nohata, Nijiro; Kinoshita, Takashi; Fuse, Miki; Seki, Naohiko; Nakagawa, Masayuki

doi:10.3892/ijo.2012.1391

Cited by 34 publications

(22 citation statements)

References 35 publications

(56 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Similar results were observed with the knockdown of miR-1 targeted gene SRSF9 [58]. In another recent study by the same group, novel molecular targets regulated by miR-1 in bladder cancer were identified [59]. Genome-wide molecular target search and luciferase reporter assays showed that prothymosin- α (PTMA) and PNP are directly regulated by miR-1.…”

Section: Aberrant Expression Of Mir-1 In Human Cancerssupporting

confidence: 65%

See 1 more Smart Citation

Role of MicroRNA-1 in Human Cancer and Its Therapeutic Potentials

Han

Duan

et al. 2014

BioMed Research International

View full text Add to dashboard Cite

While the mechanisms of human cancer development are not fully understood, evidence of microRNA (miRNA, miR) dysregulation has been reported in many human diseases, including cancer. miRs are small noncoding RNA molecules that regulate posttranscriptional gene expression by binding to complementary sequences in the specific region of gene mRNAs, resulting in downregulation of gene expression. Not only are certain miRs consistently dysregulated across many cancers, but they also play critical roles in many aspects of cell growth, proliferation, metastasis, apoptosis, and drug resistance. Recent studies from our group and others revealed that miR-1 is frequently downregulated in various types of cancer. Through targeting multiple oncogenes and oncogenic pathways, miR-1 has been demonstrated to be a tumor suppressor gene that represses cancer cell proliferation and metastasis and promotes apoptosis by ectopic expression. In this review, we highlight recent findings on the aberrant expression and functional significance of miR-1 in human cancers and emphasize its significant values for therapeutic potentials.

show abstract

Section: Aberrant Expression Of Mir-1 In Human Cancerssupporting

confidence: 65%

“…PTMA and PNP were identified as new target genes regulated by miR-1 in bladder cancer. These genes may function as oncogenes contributing to cell proliferation and invasion in bladder cancer [59]. PTMA is one of the miR-1 target genes involved in miR-1 inducing apoptosis.…”

Section: Aberrant Expression Of Mir-1 In Human Cancersmentioning

confidence: 99%

Role of MicroRNA-1 in Human Cancer and Its Therapeutic Potentials

Han

Duan

et al. 2014

BioMed Research International

View full text Add to dashboard Cite

show abstract

“…They also demonstrated that transient transfection of BC cell lines with miR-133a, miR-1, and miR-218, reduced the expression of mRNA and protein levels of LIM and SH3 protein 1 (LASP1), an actin binding protein, and reduced cell viability [30]. This group showed that miR-1 and miR-133a targets the genes encoding transgelin 2 (TAGLN2), a protein with unknown function but an observed clinical correlation with BC tumor grade [31], as well as prothymosin-α (PTMA), which is involved in cellular proliferation and differentiation, and purine nucleoside phosphorylase (PNP), an enzyme that catalyzes phosphorolysis of purine nucleosides and when deficient results in impaired cell-mediated immunity [32]. In addition, they reported that miR-1 may mediate apoptosis through inhibition of splicing factor arginine/serine-rich 9 (SRSF9/SRp30s) [33] and that miR-133a induces apoptosis via regulation of glutathione S-transferase π1 (GSTP1) where transfection of cell lines with miR-133a reduced mRNA and protein expression levels of GSTP1 [27].…”

Section: Resultsmentioning

confidence: 99%

The evolving understanding of microRNA in bladder cancer

Guancial

Bellmunt

Yeh

et al. 2014

Urologic Oncology: Seminars and Original Investigations

View full text Add to dashboard Cite

Purpose MicroRNA (miR) expression is altered in urologic malignancies, including bladder cancer (BC). Individual miRs have been shown to modulate multiple signaling pathways that contribute to BC. We reviewed the primary literature on the role of miRs in BC and provide a general introduction to the processing, regulation, and function of miRs as tumor suppressors and oncogenes; and critically evaluate the literature on the implications of altered miR expression in BC. Materials and Methods We searched the English language literature for original and review articles in PubMed® from 1993 to March 2013, using the terms “microRNA” and “bladder cancer,” “transitional cell carcinoma,” or “urothelial carcinoma.” This search yielded 133 unique articles with greater than 85% published within the last three years. Results To date, the majority of miR studies in BC use profiling to describe dynamic changes in miR expression across stage and grade. Generalized down regulation of miRs, including those that target the fibroblast growth factor 3 (FGFR3) pathway such as miR-145, miR-101, miR-100 and miR-99a, has been observed in low grade, non-muscle invasive bladder cancer (NMIBC). In contrast, generalized increased expression of miRs is observed in high grade, muscle invasive bladder cancer (MIBC) compared with adjacent normal bladder urothelium, including miRs predicted to target p53, such as miR-21 and miR-373. Furthermore, p53 suppresses transcriptional factors which promote mesenchymal differentiation, ZEB-1 and ZEB-2, through regulation of the miR200 family. Conclusions Aberrations in miR expression identified between NMIBC and MIBC support and provide insight into molecular alterations known to distinguish the two parallel pathways of bladder carcinogenesis. The heterogeneity of tumor specimens and research methods limits the reproducibility of changes in miR expression profiles between studies and underscores the importance of in vivo validation in a field that utilizes in silico miR target prediction models.

show abstract

“…There are 2,418 targets predicted for miR-630 by the miRanda algorithm and NSAID upregulation of miR-630 might thus influence on tumor growth (44). Other miRNAs, acting as tumor suppressors and frequently downregulated in human solid cancers, are miR-1, miR-133a, miR-133b and miR-206 (45–50). miR-1 and miR-133a form clusters on two chromosomes, at 20q13 and 18q11, producing mature miRs with identical sequences, while miR-206 and miR-133b are located at chromosome 6p12 (51).…”

Section: Discussionmentioning

confidence: 99%

Preoperative low dose NSAID treatment influences the genes for stemness, growth, invasion and metastasis in colorectal cancer

Lönnroth

Andersson

Asting

et al. 2014

International Journal of Oncology

View full text Add to dashboard Cite

Preclinical data, and an increasing list of clinical investigations, show anti-inflammatory agents to favourably influence the biology of colorectal tumor. We have earlier reported on re-expression of activated immune cells after three days preoperative treatment of patients with colorectal carcinoma, randomized to receive oral NSAID (indomethacin or celebrex). Antisecretory prophylaxis (esomeprasol) was provided to all patients and served as sham treatment. Concomittant to MHC locus activation, Prominin1/CD133, a marker associated with stemness and poor prognosis in several solid tumors, was downregulated. The aim of the present study was to evaluate expression of additional regulators belonging to the stem cell niche, OCT4, SOX2 and BMP7, as well as some microRNAs, reported to act as tumor suppressors or oncomiRs. Peroperative tumor biopsies were analyzed by microarrays, quantitative real-time PCR and immunohistochemistry (IHC). The stem cell master regulator SOX2 was increased by NSAIDs (p<0.01), as well as the tumor suppressor miR-630 (p<0.01), while BMP7, a marker for poor prognosis in CRC, was downregulated by NSAID (indomethacin, p<0.02). The upregulation of SOX2, but not of its heterodimer binding partner OCT4, could imply a negative feed-back loop, with a switch-off for stemness preservation of tumor cells. This is supported by the overall evaluation of gene expression profiles with subsequent events, indicating less aggressive tumors following NSAID treatment.

show abstract

Novel molecular targets regulated by tumor suppressors microRNA-1 and microRNA-133a in bladder cancer

Cited by 34 publications

References 35 publications

Role of MicroRNA-1 in Human Cancer and Its Therapeutic Potentials

Role of MicroRNA-1 in Human Cancer and Its Therapeutic Potentials

The evolving understanding of microRNA in bladder cancer

Preoperative low dose NSAID treatment influences the genes for stemness, growth, invasion and metastasis in colorectal cancer

Contact Info

Product

Resources

About