Retracted: miR-27b-3p Inhibits Invasion, Migration and Epithelial-mesenchymal Transition in
Gastric Cancer by Targeting RUNX1 and Activation of the Hippo Signaling Pathway

Bao, Chenhui; Guo, Lin

doi:10.2174/1871520621666210707095833

Cited by 14 publications

(8 citation statements)

References 68 publications

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“…studies have revealed that RUNX1 mRNA is associated with metastasis of breast and prostate cancers, with expression inversely associated with tumour aggressiveness. 15,[23][24][25][26] Moreover, RUNX1 has been reported to be involved in several hormone-related solid cancers. 26 Beyond breast cancer, overexpression of RUNX1 was suggested to play a promotive role in endometrioid carcinoma myometrial infiltration.…”

Section: Discussionmentioning

confidence: 99%

“…It is also becoming evident that varying levels of RUNX1 expression can be identified as markers of tumour progression not only in haematopoietic system diseases but also in solid tumour diseases 16,22 . Earlier studies have revealed that RUNX1 mRNA is associated with metastasis of breast and prostate cancers, with expression inversely associated with tumour aggressiveness 15,23–26 . Moreover, RUNX1 has been reported to be involved in several hormone‐related solid cancers 26 .…”

Section: Discussionmentioning

confidence: 99%

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RUNX1 promotes liver fibrosis progression through regulating TGF‐β signalling

Guo

Liu

Zhao

et al. 2023

Int J Experimental Path

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Liver fibrosis is caused by chronic liver injury. There are limited treatments for it, and the pathogenesis is unclear. Therefore, there is an urgent need to explore the pathogenesis of liver fibrosis, and to try to identify new potential therapeutic targets. For this study we used the carbon tetrachloride abdominal injection induced liver fibrosis animal model in mice. Primary hepatic stellate cell isolation was performed by a density‐gradient separation method, and this was followed by immunofluorescence stain analyses. Signal pathway analysis was performed by dual‐luciferase reporter assay and western blotting. Our results showed that RUNX1 was upregulated in cirrhotic liver tissues compared with normal liver tissues. Besides, overexpression of RUNX1 caused more severe liver fibrosis lesions than control group under CCl4‐induced conditions. Moreover, α‐SMA expression in the RUNX1 overexpression group was significantly higher than in the control group. Interestingly, we found that RUNX1 could promote the activation of TGF‐β/Smads in a dual‐luciferase reporter assay. Thus we demonstrated that RUNX1 could be considered as a new regulator of hepatic fibrosis by activating TGF‐β/Smads signalling. Based on this, we concluded that RUNX1 may be developed as a new therapeutic target in the treatment of liver fibrosis in the future. In addition, this study also provides a new insight about the aetiology of liver fibrosis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

RUNX1 promotes liver fibrosis progression through regulating TGF‐β signalling

Guo

Liu

Zhao

et al. 2023

Int J Experimental Path

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“…Similar to this finding, Zhu et al verified that miR-27b-3p is abnormally upregulated in HCC [ 51 ]. Besides, the role of miR-27b-3p is highly comparable not only in HCC but also in other tumors [ 27 , 28 , 52 ]. Furthermore, Wu et al found that miR-27b-3p downregulation causes chemoresistance in colorectal cancer (CRC), revealing the anti-cancer effect of miR-27b-3p in CRC [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

circRanGAP1/miR-27b-3p/NRAS Axis may promote the progression of hepatocellular Carcinoma

et al. 2022

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Background Though circular RNAs (circRNAs) are the key regulators in tumor carcinogenesis, they remain largely unexplored in hepatocellular carcinoma (HCC). Methods The expression of RanGAP1-derived circRNAs (circ_0063531, circ_0063534, circ_0063513, circ_0063518, circ_0063507, circ_0063723) were evaluated in eight paired HCC and normal tissues, and the correlation between circRanGAP1 (circ_0063531) expression and clinicopathological characteristics in 40 HCC patients was determined. The association between miR-27b-3p and circRanGAP1 or NRAS was predicted using bioinformatics analysis. The expression of circRanGAP1, miR-27b-3p, and NRAS were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The potential oncogenic role of circ-RanGAP1 was assessed using CCK-8, colony formation, transwell assays in vitro, subcutaneous tumor mouse model, vein tail metastatic model, and orthotopically implanted intrahepatic HCC model in vivo. Luciferase reporter and RNA immunoprecipitation (RIP) assays were used to explore the binding site between miR-27b-3p and circ-RanGAP1 or NRAS. Protein expression was detected using western blotting. The localization of miR-27b-3p and circ-RanGAP1 was investigated using fluorescence in situ hybridization (FISH). The level of immune infiltration was assessed by bioinformatics analysis, flow cytometry, and orthotopically implanted intrahepatic HCC models. Results Here, we found elevated circRanGAP1 in the cells and clinical tissues of patients with HCC. Increased circRanGAP1 levels are associated with enlarged tumors and the advanced stage of TNM. CircRanGAP1 promotes the growth, migration, and HCC cell invasion, concurrently with the growth and metastasis of tumors in-vivo. Moreover, circRanGAP1 is mainly located inside the cytoplasm. Mechanistically, circRanGAP1 as an oncogene promotes HCC progression by miR-27b-3p/NRAS/ERK axis, furthermore, affects the infiltration level of tumor-associated macrophages probably by sponging miR-27b-3p. Immune infiltration analysis shows that NRAS is positively correlated with the levels of CD68+ tumor-associated macrophages in HCC samples and that NRAS and CD68 are related to the poor outcome of HCC. Conclusion These results reveal that circRanGAP1 is a HCC oncogene that function by the miR-27b-3p/NRAS/ERK axis and regulates the infiltration levels of tumor-associated macrophages by sponging miR-27b-3p. Therefore, circRANGAP1/ NRAS axis may be an important potential treatment target against HCC.

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“…It is controversial whether abnormally expressed miR-27b-3p acts as an oncogene or an anti-oncogene in cancer. miR-27b-3p inhibited malignant progression capacity by targeting RUNX1, Nrf2, and MARCH7 in gastric cancer, esophageal squamous cell carcinoma, and endometrial cancer, respectively [ 25 – 27 ]. In contrast, miR-27b-3p accelerated tumor progression via PPARG and HOXA10 in triple-negative breast cancer and colorectal cancer, respectively [ 28 , 29 ].…”

Section: Discussionmentioning

confidence: 99%

LINC01089 blocks malignant progression of thyroid cancer by binding miR-27b-3p to enhance the FBLN5 protein level

et al. 2022

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LINC01089 suppresses the malignant progression of breast, colorectal, and non-small cell lung cancers. However, the function of LINC01089 in thyroid cancer has not yet been elucidated. Here, The Cancer Genome Atlas (TCGA) database showed that LINC01089 expression is remarkably reduced in thyroid cancer tissues. Lower LINC01089 expression was correlated with higher tumor stage and regional lymph node metastasis. Furthermore, LINC01089 overexpression effectively blocked thyroid cancer cell proliferation, migration, and invasion. LINC01089 acted as a competing endogenous RNA for miR-27b-3p, thus inhibiting miR-27b-3p expression. miR-27b-3p overexpression promoted the proliferation, migration, and invasion of thyroid cancer, reversing the effect of LINC01089 overexpression on thyroid cancer. Fibulin-5 (FBLN5) was discovered as a target of miR-27b-3p in thyroid cancer. FBLN5 expression was found to be underexpressed in thyroid cancer and was enhanced and reduced by LINC00987 overexpression and miR-27b-3p overexpression, respectively. Furthermore, FBLN5 knockdown promoted the malignant progression of thyroid cancer cells by counteracting the effect of LINC00987. In conclusion, LINC01089 plays a tumor-suppressive role by binding miR-27b-3p to increase FBLN5 expression, confirming that LINC01089 has tremendous potential to become a therapeutic target for thyroid cancer treatment.

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Retracted: miR-27b-3p Inhibits Invasion, Migration and Epithelial-mesenchymal Transition in Gastric Cancer by Targeting RUNX1 and Activation of the Hippo Signaling Pathway

Cited by 14 publications

References 68 publications

RUNX1 promotes liver fibrosis progression through regulating TGF‐β signalling

RUNX1 promotes liver fibrosis progression through regulating TGF‐β signalling

circRanGAP1/miR-27b-3p/NRAS Axis may promote the progression of hepatocellular Carcinoma

LINC01089 blocks malignant progression of thyroid cancer by binding miR-27b-3p to enhance the FBLN5 protein level

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