Let-7a inhibits growth and migration of breast cancer cells by targeting HMGA1

Liu, Kui; Zhang, Chunfu; Li, Tao; Ding, Yongsheng; Tu, Tao; Zhou, Fangfang; Qi, Wenkai; Chen, Huabiao; Sun, Xiaochun

doi:10.3892/ijo.2015.2949

Cited by 81 publications

(57 citation statements)

References 52 publications

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“…HMGA1 is primarily expressed in fetal tissues (Hynes et al, 1994) and many cancer tissues, such as colorectal cancer (Williama et al, ), breast cancer (Cianfrocca et al, ), pancreatic cancer (Piscuoglio et al, ), ovarian cancer (Liu et al, ), and prostate cancer (Zhang et al, ). In this study, we found that HMGA1 expression in breast cancer tissues was stronger than that in normal breast tissues, which is consistent with the previous reports on breast cancer cell lines and breast cancer tissues (Liu et al, ; Sepe et al, ). Furthermore, we found that HMGA1 played an important role in the progression of breast cancer.…”

Section: Discussionsupporting

confidence: 93%

HMGA1 Overexpression is Associated With the Malignant Status and Progression of Breast Cancer

Cao

et al. 2018

The Anatomical Record

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Breast cancer is the most common malignant tumor among women, and the incidence and mortality of breast cancer has rapidly increased in recent years. Studies have indicated that high mobility group A1 (HMGA1), an important member of the HMGA family, plays a role in the pathogenesis and progression of malignant tumors, including breast cancer. This study aims to evaluate the effect of HMGA1 in breast cancer. Interestingly, we found that HMGA1 expression was significantly higher in breast cancer tissues than in adenoma tissues and closely correlated with the clinical stage and histological grade in breast cancer patients. Further study showed that HMGA1 knockdown inhibited the proliferation and migration of breast cancer cells. Thus, the results demonstrated that HMGA1 could act as an independent prognostic indicator in breast cancer. HMGA1 expression was closely correlated with the clinical stage, histological grade, and tumor size in breast cancer patients and breast cancer progression in transgenic MMTV-PyMT mice. Anat Rec, 301:1061-1067, 2018. © 2018 Wiley Periodicals, Inc.

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Section: Discussionsupporting

confidence: 93%

HMGA1 Overexpression is Associated With the Malignant Status and Progression of Breast Cancer

Cao

et al. 2018

The Anatomical Record

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“…Elevated let-7 is subsequently maintained in various adult tissue [17]. In contrast, decreased expression of let-7 has been detected in human cancers, including hepatocellular carcinoma, breast cancer, and lung cancer [18][19][20], possibly indicating the reverse embryogenesis process occurs during tumorigenesis [21].…”

Section: Introductionmentioning

confidence: 99%

“…Let-7 family, including let-7d, was reported to inhibit tumor pathogenesis [20,22]. On the other hand, let-7d contributes to the pathogenesis of some cancers.…”

Section: Introductionmentioning

confidence: 99%

Let-7d Inhibits Growth and Metastasis in Breast Cancer by Targeting Jab1/Cops5

Wei

Liu

et al. 2018

Cell Physiol Biochem

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Background/Aims: MicroRNAs (miRNAs) regulate the expressions of cancer-related genes, and are involved in the development and progression of various human cancers. Here, we performed further analyses to determine whether let-7d is functionally linked to Jab1 in breast cancer. Methods: In situ hybridization and immunohistochemical analyses were used to determine the level of let-7d and Jab1 in breast cancer clinical specimens and its correlation with clinicopathological data. Let-7d overexpressing breast cancer cell lines combined with mouse models bearing cell-derived xenografts were used to assess the functional role of let-7d both in vitro and in vivo. Results: In this study, we found that let-7d was downregulated in breast cancer tissues, coupled with the elevations of Jab1 protein expressions, compared with paired adjacent noncancerous breast tissues. Let-7d overexpression significantly suppressed the proliferation and invasion in MCF-7 and MDA-MB-231 cells. Dual luciferase reporter assay indicated that Jab1 was the direct target of let-7d. Stepwise studies from in vitro and in vivo experiments indicated that let-7d overexpression inhibited cell growth and decreased Jab1 expressions in breast cancer cells and nude mice tumor tissues. Statistical analyses demonstrated that breast cancer patients with low levels of let-7d or high levels of Jab1 had a significant correlation with worse prognosis. Conclusion: These findings provide novel insights into molecular mechanism of let-7d and Jab1 in tumor development and progression of breast cancer, and thus let-7d/Jab1 are novel potential therapeutic targets for breast cancer patients.

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“…It has been reported that let‐7a is poorly expressed in glioma when compared with that of a normal healthy brain . Additionally, compared with the adjacent normal tissues, let‐7a expression is found to be reduced in breast cancer tissues . A previous study presented evidence highlighting the down‐regulation of let‐7f in glioma cells and tissues .…”

Section: Discussionmentioning

confidence: 99%

microRNA cluster MC‐let‐7a‐1~let‐7d promotes autophagy and apoptosis of glioma cells by down‐regulating STAT3

et al. 2019

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Background Accumulating evidence has highlighted the correlation between microRNAs (miRNAs) and the progression of glioma. However, the role of miR cluster MC‐let‐7a‐1 ~ let‐7d in glioma remains elusive. Thus, the current study aimed to investigate the effect of miR cluster MC‐let‐7a‐1 ~ let‐7d on glioma progression. Methods and Results Microarray data analysis provided data indicating the involvement of miR cluster MC‐let‐7a‐1 ~ let‐7d in glioma via STAT3. The expression of let‐7a‐1, let‐7d, let‐7f‐1, and miR cluster MC‐let‐7a‐1 ~ let‐7d was diminished in the glioma tissues and the cell lines. Additionally, our results revealed that STAT3 was a target gene of let‐7d, let‐7a‐1, and let‐7f‐1, which was further verified by the dual‐luciferase reporter gene assay. Moreover, STAT3 expression was negatively mediated by let‐7a‐1, let‐7d, and let‐7f‐1. Up‐regulated miR cluster MC‐let‐7a‐1 ~ let‐7d or silenced STAT3 suppressed cell proliferation but accelerated cell apoptosis and autophagy. Moreover, restrained tumor growth was identified in the nude mice treated with miR cluster MC‐let‐7a‐1 ~ let‐7d mimics or STAT3 siRNA. Conclusion Taken together, the miR cluster MC‐let‐7a‐1 ~ let‐7d promotes glioma cell autophagy and apoptosis by repressing STAT3. The current study highlights the potential of the miR cluster MC‐let‐7a‐1 ~ let‐7d as biomarkers and promising treatment strategies for glioma.

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Let-7a inhibits growth and migration of breast cancer cells by targeting HMGA1

Cited by 81 publications

References 52 publications

HMGA1 Overexpression is Associated With the Malignant Status and Progression of Breast Cancer

HMGA1 Overexpression is Associated With the Malignant Status and Progression of Breast Cancer

Let-7d Inhibits Growth and Metastasis in Breast Cancer by Targeting Jab1/Cops5

microRNA cluster MC‐let‐7a‐1~let‐7d promotes autophagy and apoptosis of glioma cells by down‐regulating STAT3

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