Deregulation of cancer-related miRNAs is a common event in both benign and malignant human breast tumors

Tahiri, Andliena; Leivonen, Suvi‐Katri; Lüders, Torben; Steinfeld, Israel; Aure, Miriam Ragle; Geisler, Jürgen; Mäkelä, Rami; Nord, Silje; Riis, Margit; Yakhini, Zohar; Sahlberg, Kristine Kleivi; Børresen-Dale, Anne Lise; Perälä, Merja; Bukholm, Ida Rashida Khan; Kristensen, Vessela N.

doi:10.1093/carcin/bgt333

Cited by 121 publications

(104 citation statements)

References 48 publications

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“…These results suggest that miR-193a-3p may be involved in the pathogenesis of lung cancer as a tumor suppressor. Indeed, miR193a-3p has been reported in many studies to be down-regulated in cancers (31,33,38,52,54,55). On the other hand, it is well known that a single miRNA can target multiple genes, whereas multiple miRNAs can target a single gene.…”

Section: Discussionmentioning

confidence: 99%

miR-193a-3p Functions as a Tumor Suppressor in Lung Cancer by Down-regulating ERBB4

Liang

Liu

Yan

et al. 2015

Journal of Biological Chemistry

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Background: ERBB4 plays an important role in the etiology and progression of lung cancer. Results: miR-193a-3p suppressed proliferation and invasion and promoted apoptosis in lung cancer cells and xenograft mice by negatively regulating ERBB4. Conclusion: miR-193a-3p exerted an anti-tumor effect by negatively regulating ERBB4 in lung cancer. Significance:This study may open new avenues for future lung cancer therapies.

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Section: Discussionmentioning

confidence: 99%

miR-193a-3p Functions as a Tumor Suppressor in Lung Cancer by Down-regulating ERBB4

Liang

Liu

Yan

et al. 2015

Journal of Biological Chemistry

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“…miR-21 has been reported to be an important oncomir in many types of cancer (32)(33)(34). Most of the studies so far focused on the increased expression of miR-21 in cancer cells or tumor mixture.…”

Section: Discussionmentioning

confidence: 99%

miR-21 Induces Myofibroblast Differentiation and Promotes the Malignant Progression of Breast Phyllodes Tumors

Gong

Nie

et al. 2014

Cancer Research

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Phyllodes tumors of breast, even histologically diagnosed as benign, can recur locally and have metastatic potential. Histologic markers only have limited value in predicting the clinical behavior of phyllodes tumors. It remains unknown what drives the malignant progression of phyllodes tumors. We found that the expression of myofibroblast markers, a-smooth muscle actin (a-SMA), fibroblast activation protein (FAP), and stromal cell-derived factor-1 (SDF-1), is progressively increased in the malignant progression of phyllodes tumors. Microarray showed that miR-21 was one of the most significantly upregulated microRNAs in malignant phyllodes tumors compared with benign phyllodes tumors. In addition, increased miR-21 expression was primarily localized to a-SMA-positive myofibroblasts. More importantly, a-SMA and miR-21 are independent predictors of recurrence and metastasis, with their predictive value of recurrence better than histologic grading. Furthermore, miR-21 mimics promoted, whereas miR-21 antisense oligos inhibited, the expression of a-SMA, FAP, and SDF-1, as well as the proliferation and invasion of primary stromal cells of phyllodes tumors. The ability of miR-21 to induce myofibroblast differentiation was mediated by its regulation on Smad7 and PTEN, which regulate the migration and proliferation, respectively. In breast phyllodes tumor xenografts, miR-21 accelerated tumor growth, induced myofibroblast differentiation, and promoted metastasis. This study suggests an important role of myofibroblast differentiation in the malignant progression of phyllodes tumors that is driven by increased miR-21. Cancer Res; 74(16); 4341-52. Ó2014 AACR.

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“…Among these miRNAs, miR-195 has been shown to act as a suppressor in various cancers (4,6); for example, miR-195 suppressed the proliferation, migration and invasion of non-small cell lung cancer by targeting MYB (7). miR-195 has also been suggested to be useful as a potential diagnostic and therapeutic target for breast cancer (8,9), and has been shown to inhibit bladder cancer cell proliferation by directly targeting CDK4 and GLUT3 (10,11). As one miRNA has multiple targets, and one mRNA can be targeted by numerous miRNAs (12), the underlying molecular mechanisms of miR-195 in bladder cancer, and the existence of other targets of miR-195, remain unclear.…”

Section: Introductionmentioning

confidence: 99%

microRNA-195 inhibits cell proliferation in bladder cancer via inhibition of cell division control protein 42 homolog/signal transducer and activator of transcription-3 signaling

Zhao¹,

Lin²,

Chen³

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. microRNA (miR)-195 acts as a suppressor in multiple types of malignant tumors, including bladder cancer; however, the detailed function of miR-195 in bladder cancer remains largely unknown. The aim of the present study was to investigate the role of miR-195 in the regulation of bladder cancer cell proliferation and to determine whether cell division control protein 42 homolog (Cdc42)/signal transducer and activator of transcription-3 (STAT3) signaling acts as a downstream effector of miR-195 in bladder cancer cells. Reverse transcription-quantitative polymerase chain reaction was used to determine the expression levels of miR-195 in bladder cancer tissues and normal adjacent tissue. The results revealed that the expression of miR-195 was significantly downregulated in bladder cancer tissues compared with that in the normal adjacent tissues. A luciferase reporter assay was then conducted, which identified Cdc42 as a direct target of miR-195, and the expression of Cdc42 was significantly upregulated in bladder cancer tissues, as determined by western blotting. Furthermore, miR-195 negatively regulated the protein expression of Cdc42 in bladder cancer cells. An MTT assay was also conducted to determine the rate of cell proliferation. Upregulation of miR-195 or the inhibition of Cdc42 could inhibit bladder cancer cell proliferation, possibly through activation of STAT3 signaling. In addition, restoration of Cdc42 could reverse the inhibitory effect of miR-195 upregulation on bladder cancer cell proliferation. In conclusion, the results of the present study suggest that miR-195 plays an inhibitory role in the regulation of bladder cancer cell proliferation by directly targeting Cdc42/STAT3 signaling.

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Deregulation of cancer-related miRNAs is a common event in both benign and malignant human breast tumors

Cited by 121 publications

References 48 publications

miR-193a-3p Functions as a Tumor Suppressor in Lung Cancer by Down-regulating ERBB4

miR-193a-3p Functions as a Tumor Suppressor in Lung Cancer by Down-regulating ERBB4

miR-21 Induces Myofibroblast Differentiation and Promotes the Malignant Progression of Breast Phyllodes Tumors

microRNA-195 inhibits cell proliferation in bladder cancer via inhibition of cell division control protein 42 homolog/signal transducer and activator of transcription-3 signaling

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