Silencing of HMGA1 expression by RNA interference suppresses growth of osteogenic sarcoma

Yuan, Shaohui; Pan, Qi; Fu, Chunjiang; Zhang, Bi

doi:10.1007/s11010-011-0865-7

Cited by 8 publications

(12 citation statements)

References 20 publications

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“…We verified the positive effects of HMGA1 on osteosarcoma cell proliferation, migration and invasion using RNA interference. Our result was similar to Yuan and colleagues' findings, who reported that silencing of HMGA1 was able to suppress osteosarcoma growth [30]. Moreover, the inhibitory effects exerted by miR-142-3p on proliferation, migration and invasion were reversed partially after HMGA1 overexpression.…”

Section: Discussionsupporting

confidence: 92%

MiR-142-3p Functions as a Potential Tumor Suppressor in Human Osteosarcoma by Targeting HMGA1

Wang

Jia

et al. 2014

Cell Physiol Biochem

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Background/Aims: Mounting evidence has shown that aberrant expression of miRNAs correlates with human cancers, and that miRNAs can function as tumor suppressors or oncogenes. Here, we investigated the role and mechanism of miR-142-3p in human osteosarcoma. Methods: We used quantitative real-time RT-PCR to measure the expression of miR-142-3p in human osteosarcoma cell lines and tissues. The roles of miR-142-3p in osteosarcoma development were studied using cultured HOS, MG63 and Saos-2 cells and tumor xenograft analyses in nude mice; their target genes were also investigated. Results: We found that miR-142-3p was significantly downregulated in osteosarcoma cell lines and clinical specimens. Overexpression of miR-142-3p suppressed osteosarcoma cell proliferation, migration and invasion, whereas miR-142-3p knockdown increased these parameters. The xenograft mouse model also revealed the suppressive effect of miR-142-3p on tumor growth. High mobility group AT-hook 1 (HMGA1) was identified as a target of miR-142-3p. Downregulation of HMGA1 induced effects on osteosarcoma cell lines similar to those induced by miR-142-3p. In contrast, restoration of HMGA1 abrogated the effects induced by miR-142-3p up-regulation. Conclusion: These results indicated that miR-142-3p may function as a tumor suppressor by targeting HMGA1 in osteosarcoma.

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Section: Discussionsupporting

confidence: 92%

MiR-142-3p Functions as a Potential Tumor Suppressor in Human Osteosarcoma by Targeting HMGA1

Wang

Jia

et al. 2014

Cell Physiol Biochem

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“…The present study also observed that a reduction in the expression of HMGA1 led to a reduced growth rate in H1299 cells. The suppression of cell growth in response to the suppressed expression of HMGA1 has also been observed in breast cancer and osteogenic sarcoma (26). …”

Section: Discussionmentioning

confidence: 92%

Expression of miR-26a exhibits a negative correlation with HMGA1 and regulates cancer progression by targeting HMGA1 in lung adenocarcinoma cells

Sekimoto

Suzuki

et al. 2016

Molecular Medicine Reports

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Lung cancer is the most common cause of cancer-associated mortality worldwide, and the number of cases is increasing annually. Several studies have shown that microRNAs (miRNAs) control proliferation, differentiation, and apoptosis in various cell types, and increasing evidence indicates the presence of aberrant miRNA expression profiles and unique miRNA signaling pathways in several types of cancer. The present study aimed to identify miRNAs, which correlated specifically with the progression of lung cancer through the analysis of 57,100 transcripts and 1,341 small RNA expression profiles in 26 lung adenocarcinoma cell lines using next-generation sequencing. The most marked negative correlation was found between the expression of hsa-miR-26a-1 and messenger RNA (mRNA), and a list of mRNAs, which exhibited negative correlation with hsa-miR-26a-1 were investigated. The most marked negative correlation was observed between the expression levels of hsa-miR-26a-1 and high mobility group A1 (HMGA1). Using a lung adenocarcinoma cell line, the present study analyzed the effect of the overexpression of miR-26a on the expression of HMGA1 and found that miR-26a repressed the expression of HMGA1 by reducing the mRNA levels of HMGA1. Furthermore, it was demonstrated that the overexpression of miR-26a in a lung adenocarcinoma cell line repressed cell migration, invasion and growth by targeting HMGA1. Taken together, the present study showed a significant negative correlation between the expression of miR-26a and HMGA1 in 26 lung adenocarcinoma cell lines, and provided evidence that the suppression of miR-26a supports the progression of cancer by stimulating the expression of HMGA1.

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“…HMGA1 inhibits the function of p53 family members in thyroid cancer cells, increases the expression of oncogenic miR-222 in lung cancer cells, enhances cancer cell resistance to genotoxic agents, enhances epithelial-mesenchymal transition, and promotes tumor progression in breast cancer cells [25,[38][39][40]. Recent study has shown HMGA1 upregulation to be associated with survival in pancreatic ductal adenocarcinoma whereas downregulation of HMGA1 has enhanced gemcitabine chemosensitivity for suppressing growth of tumor cells [26,41,42]. Our study has showed that HMGA1 as an architectural transcription factor was expressed in gliomas but not expressed in normal human brain tissue, that HMGA1 expression in GM was higher than in WHO grade II and III gliomas, and that overexpression of HMGA1 was closely correlated with high levels of Ki67, MVD, VEGF-A, and MMP-9, which were related to tumor progression.…”

Section: Discussionmentioning

confidence: 99%

HMGA1 expression in human gliomas and its correlation with tumor proliferation, invasion and angiogenesis

et al. 2011

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High-mobility group A1 (HMGA1) protein is an architectural transcription factor widely expressed during embryonic development and tumor progression. The purpose of this research was to investigate the expression of HMGA1 in malignant gliomas with different WHO classification and to study the correlation of HMGA1 expression with tumor proliferation, invasion, and angiogenesis. Expression of HMGA1, Ki-67, MMP-9, VEGF-A, and MVD in malignant gliomas and their correlation were studied in 60 samples of different WHO classification by use of immunohistochemistry, and in 27 randomly selected samples by use of real-time quantitative PCR. Immunohistochemistry results showed that nuclear immunostaining of HMGA1 protein was not observed in normal brain tissues but was observed in 96.7% (58 of 60) of malignant gliomas including high (+++) in 15 (25.0%), moderate (++) in 28 (46.7%), and negligible to low (0-+) in 17 (28.3%) samples. Expression of HMGA1 protein was significantly higher in glioblastoma multiforme than in WHO grade II (P = 0.002) and WHO grade III gliomas (P = 0.024). HMGA1 protein expression correlated significantly with expression of Ki-67 (r = 0.530, P = 0.000), MMP-9 (r = 0.508, P = 0.000), VEGF-A (r = 0.316, P = 0.014), and MVD (r = 0.321, P = 0.012), but not with sex (r = 0.087, P = 0.510) and age (r = -0.121, P = 0.358). Real-time quantitative PCR results, also, were indicative of HMGA1 overexpression in glioblastoma multiforme compared with WHO grade II (P = 0.043) and WHO grade III (P = 0.031) gliomas. HMGA1 gene expression correlated significantly with gene expression of Ki-67 (r = 0.429, P = 0.025), MMP-9 (r = 0.443, P = 0.024), and VEGF-A (r = 0.409, P = 0.034). These results indicated that expression of HMGA1 correlates significantly with malignancy, proliferation, invasion, and angiogenesis of gliomas. We conclude that HMGA1 may be a potential biomarker and rational therapeutic target for human tumors.

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Silencing of HMGA1 expression by RNA interference suppresses growth of osteogenic sarcoma

Cited by 8 publications

References 20 publications

MiR-142-3p Functions as a Potential Tumor Suppressor in Human Osteosarcoma by Targeting HMGA1

MiR-142-3p Functions as a Potential Tumor Suppressor in Human Osteosarcoma by Targeting HMGA1

Expression of miR-26a exhibits a negative correlation with HMGA1 and regulates cancer progression by targeting HMGA1 in lung adenocarcinoma cells

HMGA1 expression in human gliomas and its correlation with tumor proliferation, invasion and angiogenesis

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