Induction of microRNAome deregulation in rat liver by long-term tamoxifen exposure

Pogribny, Igor P.; Tryndyak, Volodymyr; Boyko, Alex; Rodriguez-Juarez, Rocio; Beland, Frederick A.; Kovalchuk, Olga

doi:10.1016/j.mrfmmm.2006.12.006

Cited by 124 publications

(77 citation statements)

References 43 publications

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“…The induction of miR-34a by ADR treatment led us to hypothesize that miR-34a is a responsive gene for chemically induced cellular stress. This hypothesis is supported by recent reports that miR-34a is up-regulated by treatment with sodium arsenite in human immortalized lymphoblasts (19) and with tamoxifen in rat hepatocytes (20).…”

Section: Discussionsupporting

confidence: 74%

Tumor-suppressive miR-34a induces senescence-like growth arrest through modulation of the E2F pathway in human colon cancer cells

Tazawa¹,

Tsuchiya²,

Izumiya³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

882

711

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Accumulating evidence suggests a role for microRNAs in human carcinogenesis as novel types of tumor suppressors or oncogenes. However, their precise biological role remains largely elusive. In the present study, we aimed to identify microRNA species involved in the regulation of cell proliferation. Using quantitative RT-PCR analysis, we demonstrated that miR-34a was highly up-regulated in a human colon cancer cell line, HCT 116, treated with a DNAdamaging agent, adriamycin. Transient introduction of miR-34a into two human colon cancer cell lines, HCT 116 and RKO, caused complete suppression of cell proliferation and induced senescencelike phenotypes. Moreover, miR-34a also suppressed in vivo growth of HCT 116 and RKO cells in tumors in mice when complexed and administered with atelocollagen for drug delivery. Gene-expression microarray and immunoblot analyses revealed down-regulation of the E2F pathway by miR-34a introduction. Up-regulation of the p53 pathway was also observed. Furthermore, 9 of 25 human colon cancers (36%) showed decreased expression of miR-34a compared with counterpart normal tissues. Our results provide evidence that miR-34a functions as a potent suppressor of cell proliferation through modulation of the E2F signaling pathway. Abrogation of miR-34a function could contribute to aberrant cell proliferation, leading to colon cancer development.microRNA ͉ p53 ͉ adriamycin ͉ atelocollagen

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Section: Discussionsupporting

confidence: 74%

Tumor-suppressive miR-34a induces senescence-like growth arrest through modulation of the E2F pathway in human colon cancer cells

Tazawa¹,

Tsuchiya²,

Izumiya³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

882

711

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show abstract

“…[5][6][7][8] These findings suggest that expression profiling of miRNAs is an alternative method for cancer subtype classification, prognostication, and treatment. 5,7,8 It is known that HCC develops several years after HBV infection. 2,9 A p21-HBx transgenic mouse model was established by introducing the HBx gene into the p21 locus.…”

mentioning

confidence: 96%

“…5 Recent studies implicate miRNAs in several cancers, and altered miRNA levels can result in aberrant expression of gene products that may contribute to cancer biology, including tumor metastasis. [5][6][7][8] These findings suggest that expression profiling of miRNAs is an alternative method for cancer subtype classification, prognostication, and treatment. 5,7,8 It is known that HCC develops several years after HBV infection.…”

mentioning

confidence: 99%

Up‐regulated microRNA‐143 transcribed by nuclear factor kappa B enhances hepatocarcinoma metastasis by repressing fibronectin expression†

et al. 2009

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It is increasingly clear that hepatocellular carcinoma (HCC) has a distinct microRNA (miRNA) expression profile that is involved in malignancy; however, little is known about how functional miRNA modulates the metastasis of hepatitis B virus (HBV)-related HCC (HBV-HCC). In the present study, we demonstrate that the levels of miRNA-143 (miR-143) are dramatically increased in metastatic HBV-HCC of both p21-HBx transgenic mice and HCC patients. Moreover, we show that overexpression of this miRNA is transcribed by nuclear factor kappa B (NF-B) and favors liver tumor cell invasive and metastatic behavior. H epatocellular carcinoma (HCC) is a common and aggressive cancer that is strongly associated with chronic infection by the hepatitis B virus (HBV). 1 Poor prognosis and patient survival with HCC are largely due to invasion/metastasis and postsurgical recurrence. 2 The HBV X protein (HBx), a protein encoded by HBV, is thought to play a key role in the molecular pathogenesis of HBV-related HCC (HBV-HCC). 2,3 Invasion and metastasis are fundamental properties of HBV-HCC, which has a very high mortality rate. Alteration of some adhesion molecules in HBV-HCC has been described, including up-regulation of matrix metalloproteinases 1-3 and down-regulation of E-cadherin. Both of these changes indicate that HBx contributes to the metastatic spread of liver tumors. 2,4 Metastasis is a complex cascade, however, and the underlying molecular mechanisms are far from being fully understood.MicroRNAs (miRNAs) are evolutionarily endogenous regulatory noncoding RNAs that play critical roles in gene regulation. 5 Recent studies implicate miRNAs in several cancers, and altered miRNA levels can result in aberrant expression of gene products that may contribute to cancer biology, including tumor metastasis. [5][6][7][8] These findings suggest that expression profiling of miRNAs is an alternative method for cancer subtype classification, prognostication, and treatment. 5,7,8 It is known that HCC develops several years after HBV infection. 2,9 A p21-HBx transgenic mouse model was established by introducing the HBx gene into the p21 locus. About 60% of p21-HBx transgenic mice develop hepato-

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“…A miRNA detection signal threshold was defined as twice the maximum background signal. Normalization was performed with a cyclic LOWESS (locally weighted regression) method to remove system-related variations, as previously described [olstad et al, 2003;Pogribny et al, 2007]. Data adjustments included data-filtering, log 2 transformation, gene centering, and normalization.…”

Section: Mirna Microarray Expression Analysismentioning

confidence: 99%

Radiation‐induced bystander effects in vivo are epigenetically regulated in a tissue‐specific manner

Ilnytskyy

Koturbash

Kovalchuk

2008

Environ and Mol Mutagen

Self Cite

113

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Exposure of animal body parts to ionizing radiation (IR) can lead to molecular changes in distant shielded “bystander” tissues and organs. Nevertheless, tissue specificity of bystander responses within the same organism has not been examined in detail. Studies on in vivo bystander effect conducted so far analyzed changes induced by single‐dose exposure. The potential of fractionated irradiation to induce bystander effects in vivo has never been studied. We analyzed changes in global DNA methylation and microRNAome in skin and spleen of animals subjected to single‐dose (acute or fractionated) whole‐body or cranial exposure to 0.5 Gy of X‐rays. We found that IR‐induced DNA methylation changes in bystander spleen and skin were distinct. Acute radiation exposure resulted in a significant loss of global DNA methylation in the exposed and bystander spleen 6 hr, 96 hr, and 14 days after irradiation. Fractionated irradiation led to hypomethylation in bystander spleen 6 hr after whole‐body exposure, and 6 hr, 96 hr, and 14 days after cranial irradiation. Contrarily, changes in the skin of the same animals were seen only 6 hr after acute whole‐body and head exposure. DNA hypomethylation observed in spleen was paralleled by a reduction of methyl‐binding protein MeCP2 expression. Irradiation also induced tissue‐specific microRNAome alterations in skin and spleen. For the first time, we have shown that IR‐induced epigenetic bystander effects that occur in the same organism are triggered by both acute and fractionated exposure and are very distinct in different bystander organs. Future studies are clearly needed to address organismal and carcinogenic repercussions of those changes. Environ. Mol. Mutagen., 2009. © 2008 Wiley‐Liss, Inc.

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Induction of microRNAome deregulation in rat liver by long-term tamoxifen exposure

Cited by 124 publications

References 43 publications

Tumor-suppressive miR-34a induces senescence-like growth arrest through modulation of the E2F pathway in human colon cancer cells

Tumor-suppressive miR-34a induces senescence-like growth arrest through modulation of the E2F pathway in human colon cancer cells

Up‐regulated microRNA‐143 transcribed by nuclear factor kappa B enhances hepatocarcinoma metastasis by repressing fibronectin expression†

Radiation‐induced bystander effects in vivo are epigenetically regulated in a tissue‐specific manner

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