LncRNA KCNQ1OT1 knockdown inhibits viability, migration and epithelial-mesenchymal transition in human lens epithelial cells via miR-26a-5p/ITGAV/TGF-beta/Smad3 axis

Li, Jiajia; Dong, Yiran; Yang, Wen; Shi, Lei; Zhang, Zhu; Ke, Genjie; Gu, Yonghao

doi:10.1016/j.exer.2020.108251

Cited by 19 publications

(13 citation statements)

References 39 publications

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“…In addition, the concentration of TGF-β2 was much higher than that of TGF-β1 and TGF-β3, which indicated that TGF-β2 might play an important role in the mechanism of diabetes and cataracts. TGF-β2 is related to fibrosis of lens epithelial cells promoted by advanced glycation end product formation [ 19 ] and is involved in several signalling pathways activated in epithelial–mesenchymal transition, such as the MAPK/ERK/JNK and PI3K/Akt/GSK3β pathways, Jagged-1/Notch signalling, and the miR-26a-5p/ITGAV/TGF-β/Smad3 axis [ 20 – 22 ]. Besides, TGF-β1 and -β2 were correlated with glycosylated haemoglobin, which indicated that TGF-β1 and -β2 might have important roles in diabetes and diabetes related complications.…”

Section: Discussionmentioning

confidence: 99%

“…For example, high expression of miR-551b could downregulate CRYAA expression, thus decreasing the transparency of the lens [ 26 ], and low expression of miR-29b could upregulate CACNA1C expression, resulting in an increased concentration of Ca 2+ in the AH of DMC eyes [ 27 ]. The miR-26a-5p/ITGAV/TGF-β/Smad3 axis was also reported to be involved in cell viability, migration and epithelial–mesenchymal transition in diabetic cataracts [ 22 ]. These results indicated that increased TGF-β in the AH of DMC eyes might be activated by other factors, such as exosomal miRNAs, which might have important roles in the formation and development of diabetes and cataracts.…”

Section: Discussionmentioning

confidence: 99%

“…Jagged-1/Notch signalling was reported to be activated in TGF-β2-stimulated epithelial–mesenchymal transition, and blockade of Notch signalling reversed lens epithelial cell epithelial–mesenchymal transition and lens fibrosis [ 21 ]. The miR-26a-5p/ITGAV/TGF-β/Smad3 axis was also reported to be involved in cell viability, migration and epithelial–mesenchymal transition in diabetic cataracts [ 22 ]. TGF-β was additionally reported to function in promoting epithelial–mesenchymal transition of lens epithelial cells under high glucose conditions, and the c-Src/TGF-β signalling axis in the epithelial–mesenchymal transition of lens epithelial cells might be a potential novel therapeutic target for the prevention of diabetic subcapsular cataracts [ 23 ].…”

Section: Introductionmentioning

confidence: 99%

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Status of higher TGF-β1 and TGF-β2 levels in the aqueous humour of patients with diabetes and cataracts

et al. 2022

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Background Transforming growth factor (TGF) is a cytokine that acts on the proliferation, migration, differentiation, and apoptosis of cells and the accumulation of extracellular matrix components. Very few studies have precisely evaluated the concentration of TGF-β in the aqueous humour (AH) of diabetic and cataract (DMC) eyes due to the low expression of proteins in the AH or other reasons. The concentrations of TGF-β1, -β2, and -β3 in the AH of the DMC group were compared with those of the age-related cataract (ARC) group. Methods We collected AH and lens epithelium samples from 33 DMC patients and 36 ARC patients. Luminex liquid suspension chip detection was applied to detect the concentration of TGF-β1, -β2, and -β3 in the AH samples. The expression of TGFB1/2/3 in lens epithelium samples was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Results The concentrations of TGF-β1 and TGF-β2 in AH samples of DMC eyes were higher than those of ARC eyes. The differences in TGF-β1 and TGF-β2 between the two groups were statistically significant (P value = 0.001 for TGF-β1, P value = 0.023 for TGF-β2). The difference of the correlation between TGF-β1 and glycosylated haemoglobin was significant (P value = 0.011, and Pearson correlation coefficient = 0.306). The difference of the correlation between TGF-β2 and glycosylated haemoglobin was significant (P value = 0.026, and Pearson correlation coefficient = 0.269). The mRNA expression levels of TGFB1 and TGFB2 were upregulated in DMC epithelium samples compared with ARC epithelium samples. The differences in TGFB1 and TGFB2 between the two groups were statistically significant (P value for TGFB1 = 0.041, P value for TGFB2 = 0.021). Conclusions The concentrations of TGF-β1 and TGF-β2 in AH samples were significantly higher in DMC eyes than in ARC eyes. The higher the glycosylated haemoglobin was, the higher the concentrations of TGF-β1 and -β2 were. The mRNA expression of TGFB1 and TGFB2 was significantly upregulated in DMC epithelial samples compared with ARC epithelial samples, suggesting the proinflammatory status of the anterior chamber of DMC eyes.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Status of higher TGF-β1 and TGF-β2 levels in the aqueous humour of patients with diabetes and cataracts

et al. 2022

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“…KCNQ1OT1 is overexpressed in many human tumors, including liver cancer [ 11 ], colon cancer [ 26 ], acute myeloid leukemia [ 27 ], and lung cancer [ 28 ]. KCNQ1OT1 can affect the invasion of cancer cells by regulating the EMT process related to cell invaders [ 29 , 30 ]. KCNQ1OT1 was reported to be significantly more expressed in osteosarcoma than in adjacent tissues.…”

Section: Discussionmentioning

confidence: 99%

lncRNA KCNQ1OT1 Promotes EMT, Angiogenesis, and Stemness of Pituitary Adenoma by Upregulation of RAB11A

Ren

Wang

et al. 2022

Journal of Oncology

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This study is aimed at investigating the effect and mechanism of long noncoding RNA (lncRNA) KCNQ1OT1 on pituitary adenoma (PA). The KCNQ1OT1 expression in invasive and noninvasive PA tissues was detected by real-time fluorescence quantitative polymerase chain reaction (qPCR). The effects of KCNQ1OT1 on the proliferation of PA cells, namely, GH3 and HP75, were detected by CCK-8 experiment. The Transwell assay detected the effect of KCNQ1OT1 on the invasion of GH3 and HP75 cells. The effect of KCNQ1OT1 on the clonal formation ability was detected by clonal formation experiment. The double luciferase reporter assay and the miRNA pull down assay verified the binding of KCNQ1OT1 to miR-140-5p. Meanwhile, the regulatory effect of miR-140-5p on RAB11A was verified. qPCR results showed that KCNQ1OT1 was significantly increased in invasive PA compared with noninvasive PA tissues. Knockdown KCNQ1OT1 inhibited PA cell stemness, angiogenesis, and EMT. In addition, knockdown KCNQ1OT1 inhibited the proliferation, invasion, and clonal formation of PA. miR-140-5p is the target gene of KCNQ1OT1. miR-140-5p targets RAB11A directly. RAB11A can mediate the biological effects of KCNQ1OT1. Meanwhile, lncRNA KCNQ1OT1 can promote the EMT and cellular stemness of PA. Its mechanism of action is realized by inhibiting miR-140-5p. This result can provide a molecular basis for the further study of PA.

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“…They lastly proposed that silencing KCNQ1OT1 can inhibit the viability, migration and epithelial–mesenchymal transition (EMT) of lens epithelial cells. 60 Given the mentioned studies, KCNQ1OT1 was proven a vital biological indicator and a regulatory factor for diabetic patients.…”

Section: Molecular Mechanisms and Pathogenic Roles Of Lncrna Kcnq1ot1...mentioning

confidence: 99%

LncRNA KCNQ1OT1: Molecular mechanisms and pathogenic roles in human diseases

et al. 2022

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LncRNA KCNQ1OT1 knockdown inhibits viability, migration and epithelial-mesenchymal transition in human lens epithelial cells via miR-26a-5p/ITGAV/TGF-beta/Smad3 axis

Cited by 19 publications

References 39 publications

Status of higher TGF-β1 and TGF-β2 levels in the aqueous humour of patients with diabetes and cataracts

Status of higher TGF-β1 and TGF-β2 levels in the aqueous humour of patients with diabetes and cataracts

lncRNA KCNQ1OT1 Promotes EMT, Angiogenesis, and Stemness of Pituitary Adenoma by Upregulation of RAB11A

LncRNA KCNQ1OT1: Molecular mechanisms and pathogenic roles in human diseases

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