SiRNA-HMGA2 weakened AGEs-induced epithelial-to-mesenchymal transition in tubular epithelial cells

Bai, Yi-Hua; Wang, Jia-Ping; Yang, Min; Zeng, Yi Arial; Jiang, Hongying

doi:10.1016/j.bbrc.2015.01.063

Cited by 12 publications

(15 citation statements)

References 19 publications

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“…We also found that the expression of HMGA2 mRNA in the prostate cancer tissues from patients with positive lymph node metastasis or with high Gleason grade was significantly higher than that from patients with negative lymph node metastasis or with low Gleason grade. The expression level of HMGA2 was higher in gastric cancer and was closely associated with occurrence of epithelial-to-mesenchymal transition (EMT), which is involved in the metastatic process [10,15]. HMGA2 knockdown could reduce gastric cancer MKN28 cell migration and invasion [10].…”

Section: Discussionmentioning

confidence: 99%

“…The expression of HMGA2 is closely related to EMT. HMGA2 displays highlevel expression, and E-cadherin and vimentin display lowlevel expression or lost, which may suggest high degree malignancy of cancer [15]. Thuault et al found that HMGA2 and Smad3/4 can form a protein complex transcriptionally inhibiting the expression of E-cadherin and then promoting the occurrence of EMT phenotype [16].…”

Section: Introductionmentioning

confidence: 98%

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Downregulation of HMGA2 inhibits cellular proliferation and invasion, improves cellular apoptosis in prostate cancer

et al. 2015

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Prostate cancer is the most commonly diagnosed cancer among men and is the second leading cause of cancer-associated deaths among men in the world. Unfortunately, treatment failures are common due to the metastasis and chemoresistance, but the underlying molecular mechanism remains unclear. Accumulating evidence has indicated that the deregulation of DNA-binding protein High Mobility Group A2 (HMGA2) is associated with the development and progression of cancer. This study aimed to explore the expression of HMGA2 in prostate cancer tissues and its correlation to the clinical pathology of prostate cancer, and to discuss the role of HMGA2 in the development of prostate cancer. The results showed that the expression of HMGA2 messenger RNA (mRNA) in the prostate cancer tissues and cells was significantly higher than that in normal prostate tissues and cells (p < 0.05), and the positive expression rate of HMGA2 mRNA in the prostate cancer tissues from patients with positive lymph node metastasis or with high Gleason grade was significantly higher than that from patients with negative lymph node metastasis or with low Gleason grade (p < 0.05). In order to explore the role of HMGA2 in prostate cancer, the expression of HMGA2 in the human prostate cancer PC3 cell line was downregulated by RNA interference. Then, the changes in proliferation, apoptosis, invasion, and migration of PC3 cells were examined by MTT test, PI staining, Annexin V-FITC staining, and Transwell chamber assay. Results showed that the abilities of proliferation, invasion, and migration were suppressed in HMGA2 knockdown PC3 cells, and the abilities of apoptosis were enhanced in HMGA2 knockdown PC3 cells. The expression of cyclin A and vimentin was downregulated in HMGA2 knockdown PC3 cells, and the expression of caspase 3 and E-cadherin was upregulated in HMGA2 knockdown PC3 cells. Taken together, the overexpression of HMGA2 in prostate cancer might be related to the tumorigenesis, invasion, and metastasis of prostate cancer, the downregulation of HMGA2 could inhibit cellular proliferation, invasion, and metastasis, and improve cellular apoptosis in prostate cancer, which might be a potential target for the treatment of prostate cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

Downregulation of HMGA2 inhibits cellular proliferation and invasion, improves cellular apoptosis in prostate cancer

et al. 2015

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“…The ectopic expression of HMGA2 in epithelial cells induces epithelial-mesenchymal transition (EMT), which has been implicated in the acquisition of metastatic characteristics in tumor cells 30. Notably, several studies have reported that HMGA2 plays a important role in EMT during diabetic nephropathy,31,32 indicating a potential role of HMGA2 in EMT of renal cancer cells. This may occur through activation of the Wnt/β-catenin pathway,28–30,33 or through the regulation of the transcription factors involved in EMT including Snail, Slug, and Twist 30,31.…”

Section: Discussionmentioning

confidence: 99%

“…Notably, several studies have reported that HMGA2 plays a important role in EMT during diabetic nephropathy,31,32 indicating a potential role of HMGA2 in EMT of renal cancer cells. This may occur through activation of the Wnt/β-catenin pathway,28–30,33 or through the regulation of the transcription factors involved in EMT including Snail, Slug, and Twist 30,31. Besides, HMGA2 can also induce EMT through an interaction via the TGFβ signaling pathway that has been strongly implicated in EMT induction for a number of cell types both in vitro and in vivo 30,34,35.…”

Section: Discussionmentioning

confidence: 99%

High expression of HMGA2 predicts poor survival in patients with clear cell renal cell carcinoma

Na¹,

Si²,

Huang³

et al. 2016

OTT

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High-mobility group AT-hook 2 (HMGA2) is involved in a wide spectrum of biological processes and is upregulated in several tumors, but its role in renal carcinoma remains unclear. The aim of this study was to examine the expression of HMGA2 and its relationship to the overall survival (OS) of patients with non-metastatic clear cell renal cell carcinoma (ccRCC) following surgery. The expression of HMGA2 was evaluated retrospectively by immunohistochemistry (IHC) in 162 patients with ccRCC who underwent nephrectomy in 2003 and 2004. An IHC analysis revealed that HMGA2 was expressed in the nuclei of tumor cells in 146 (90.1%) patients with ccRCC. The level of HMGA2 was positively correlated with tumor size, lymph node metastasis, and Fuhrman Grade. A Kaplan–Meier analysis with log-rank test found that patients with high HMGA2 expression had a poor outcome and that patients with low HMGA2 expression had better survival. Cox regression analysis showed that HMGA2 expression could serve as an independent prognostic factor for ccRCC patients. The efficacy of the following prognostic models was improved when HMGA2 expression was added: tumor node metastasis stage, UCLA Integrated Scoring System, Mayo Clinic stage, size, grade, and necrosis score. In summary, this study showed that HMGA2 expression is an independent prognostic factor for OS in patients with ccRCC. HMGA2 was found to be a valuable biomarker for ccRCC progression.

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“…Furthermore, high glucose-induced phenotypic transition in podocytes is provoked by PTEN/PI3K/Akt pathway (29). High-mobility group AT-hook 2 (HMGA2) plays an important role in EMT during DKD, as well (30).…”

Section: Other Mediatorsmentioning

confidence: 99%

Epithelial and endothelial mesenchymal transition and their role in diabetic kidney disease

Dadras¹,

Sheikh²,

Khoshjou³

2017

J Renal Inj Prev

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Diabetes and its complications including diabetic nephropathy are spreading worldwide. On the other hand, pathophysiology of diabetic kidney disease and its modifiers have been studied broadly. This mini-review presents a couple of them, allocated to EMT and Endomt, briefly and to the point. Diabetic nephropathy (DN) is the main cause of end-stage renal disease. On the other hand, there are a couple of evidences, including human studies, which prove the role of epithelial mesenchymal transition (EMT) in pathophysiology of DN. EMT is characterized by loss of epithelial proteins and gain of mesenchymal markers. EMT is induced via three main conduit; TGFβ/Smad, integrin /ILK as well as Wnt/β-catenin pathways. Besides, numerous studies illustrated how drugs and agents can modify this phenomenon. On the other hand, endothelial mesenchymal transition (EndoMT) has a well-known role in pathophysiology of diabetic nephropathy which has been studied in animal and human. Here, several drugs and modifiers which have been studied to ffigure out if they can amend nature of EMT or EndoMT are reported briefly. Please cite this paper as:

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SiRNA-HMGA2 weakened AGEs-induced epithelial-to-mesenchymal transition in tubular epithelial cells

Cited by 12 publications

References 19 publications

Downregulation of HMGA2 inhibits cellular proliferation and invasion, improves cellular apoptosis in prostate cancer

Downregulation of HMGA2 inhibits cellular proliferation and invasion, improves cellular apoptosis in prostate cancer

High expression of HMGA2 predicts poor survival in patients with clear cell renal cell carcinoma

Epithelial and endothelial mesenchymal transition and their role in diabetic kidney disease

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