MicroRNA-10a is Overexpressed in Human Pancreatic Cancer and Involved in Its Invasiveness Partially via Suppression of the HOXA1 Gene

Ohuchida, Kenoki; Mizumoto, Kazuhiro; Chen, Lin; Yamaguchi, Hiroshi; Ohtsuka, Takao; Sato, Norihiro; Toma, Hiroki; Nakamura, Masafumi; Nagai, Eishi; Hashizume, Makoto; Tanaka, Masao

doi:10.1245/s10434-012-2252-3

Cited by 102 publications

(79 citation statements)

References 34 publications

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“…Several miRNAs that were downregulated by Gal-9 treatment have been reported to be associated with cancer cell apoptosis. For instance, miR-10a has been reported to be upregulated in several solid tumors including pancreatic cancer (35) and lung cancer (36). miR-10a targets the phosphatase and tensin homolog (PTEN), and miR-10a promotes the migration, invasion, and growth of non-small cell lung cancer by regulating the PTEN/AKT/ERK signaling pathway (36).…”

Section: Discussionmentioning

confidence: 99%

Galectin-9: An anticancer molecule for gallbladder carcinoma

Tadokoro

Morishita

Fujihara

et al. 2016

International Journal of Oncology

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Abstract. Gallbladder cancer (GBC) is the most common and aggressive type of biliary tract cancer. There are various histological types of GBC, and the vast majority of GBC cases are adenocarcinomas. Squamous and adenosquamous carcinomas are rare GBC subtypes that are traditionally considered to be more aggressive and to be associated with a poorer prognosis than adenocarcinoma. Galectin-9 (Gal-9), a tandem-repeattype galectin, has been reported to induce apoptosis-mediated elimination of various cancers, including hepatocellular carcinoma, cholangiocarcinoma, and hematologic malignancies. Therefore, we investigated the antitumor effects of Gal-9 on GBC in vitro and in vivo. In our in vitro experiments, Gal-9 suppressed cell proliferation in various GBC cell lines but not in the OCUG-1 cell line, which represents a poorly differentiated type of adenosquamous carcinoma. Gal-9 induced the apoptosis of Gal-9-sensitive GBC cells by increasing the levels of caspase-cleaved keratin 18 and phosphorylated p53. However, Gal-9 did not affect the expression of various cell cycle-related proteins. In addition, Gal-9 suppressed tumor growth by implanted human GBC cells in a xenograft model. Furthermore, Gal-9 induced the phosphorylation of the Ephrin type-B receptor, and the microRNA (miRNA) expression profile was markedly altered by Gal-9. Based on these results, various miRNAs might contribute to the suppression of tumor growth. Our data reveal that Gal-9 suppresses the growth of GBC, possibly by inducing apoptosis and altering miRNA expression. Thus, Gal-9 might serve as a therapeutic agent for the treatment of GBC.

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Section: Discussionmentioning

confidence: 99%

Galectin-9: An anticancer molecule for gallbladder carcinoma

Tadokoro

Morishita

Fujihara

et al. 2016

International Journal of Oncology

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“…Studies have established a pro-proliferative role for this cluster in multiple cancers including pancreatic cancer and acute myeloid leukemia [150][151][152]. This role is consistent with our finding that it positively regulates activation of a TF known for its role in promoting proliferation, particularly in the context of cancer [147].…”

Section: Ap-1supporting

confidence: 91%

Augmentation of Ras-induced cell transformation : a new role for miR-200a in malignancy.

Becker¹,

Erin²

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“…Overexpression of miR-10a contributes to the enhanced invasiveness in pancreatic cancer through suppression of the HOXA1 gene. 12) Higher expression of miR-10a may be also associated with an adverse outcome in breast cancer. 13) Moreover, it was reported that miR-10a can regulate the proliferation of human cardiomyocyte progenitor cells.…”

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confidence: 99%

microRNA-10a Targets T-box 5 to Inhibit the Development of Cardiac Hypertrophy

Wang

Zhai

et al. 2017

Int. Heart J.

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SummaryThe mechanism of cardiac hypertrophy involving microRNAs (miRNAs) is attracting increasing attention. Our study aimed to investigate the role of miR-10a in cardiac hypertrophy development and the underlying regulatory mechanism.Transverse abdominal aortic constriction (TAAC) surgery was performed to establish a cardiac hypertrophy rat model, and angiotensin II (AngII) was used to induce cardiac hypertrophy in cultured neonatal rat cardiomyocytes. Expression of T-box 5 (TBX5) and miR-10a was altered by cell transfection of siRNA or miRNA mimic/inhibitor. Leucine incorporation assay, histological and cytological examination, quantitative real-time PCR (qRT-PCR), and Western blot were performed to detect the effects of miR-10a and TBX5 on cardiac hypertrophy. Dual-luciferase reporter assay was conducted to verify the regulation of TBX5 by miR-10a.miR-10a was down-regulated, and TBX5 was up-regulated in the rat model and AngII-stimulated cardiomyocytes. miR-10a inhibited TBX5 expression by directly targeting the binding site in Tbx5 3'UTR. Overexpression of miR-10a in AngII-treated cardiomyocytes decreased relative cell area, and significantly reduced the mRNA levels of natriuretic peptide A (Nppa), myosin heavy chain 7 cardiac muscle beta (Myh7), and leucine incorporation (P < 0.01 or P < 0.001). Knockdown of Tbx5 had similar effects on AngII-induced cardiomyocytes.Our findings indicate that miR-10a may inhibit cardiac hypertrophy via targeting Tbx5. Thus, miR-10a provides promising therapeutic strategies for the treatment of cardiac hypertrophy. (Int Heart J 2017; 58: 100-106)

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MicroRNA-10a is Overexpressed in Human Pancreatic Cancer and Involved in Its Invasiveness Partially via Suppression of the HOXA1 Gene

Abstract: The present data suggest that miR-10a is overexpressed in a subset of pancreatic cancers and is involved in the invasive potential of pancreatic cancer cells partially via suppression of HOXA1.

Cited by 102 publications

References 34 publications

Galectin-9: An anticancer molecule for gallbladder carcinoma

Galectin-9: An anticancer molecule for gallbladder carcinoma

Augmentation of Ras-induced cell transformation : a new role for miR-200a in malignancy.

microRNA-10a Targets T-box 5 to Inhibit the Development of Cardiac Hypertrophy

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