Retracted: Circ‐SPECC1 modulates TGFβ2 and autophagy under oxidative stress by sponging miR‐33a to promote hepatocellular carcinoma tumorigenesis
Abstract Circular RNAs (circRNAs) play vital roles in the pathogenesis and development of multiple cancers, including hepatocellular carcinoma (HCC). Nevertheless, the regulatory mechanisms of circ‐SPECC1 in HCC remain poorly understood. In our study, we found that circ‐SPECC1 was apparently downreg...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2020-08-01
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| Series: | Cancer Medicine |
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| Online Access: | https://doi.org/10.1002/cam4.3219 |
| _version_ | 1797387134128095232 |
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| author | Bin Zhang Zhiyi Liu Kuan Cao Wengang Shan Jin Liu Quan Wen Renhao Wang |
| author_facet | Bin Zhang Zhiyi Liu Kuan Cao Wengang Shan Jin Liu Quan Wen Renhao Wang |
| author_sort | Bin Zhang |
| collection | DOAJ |
| description | Abstract Circular RNAs (circRNAs) play vital roles in the pathogenesis and development of multiple cancers, including hepatocellular carcinoma (HCC). Nevertheless, the regulatory mechanisms of circ‐SPECC1 in HCC remain poorly understood. In our study, we found that circ‐SPECC1 was apparently downregulated in H2O2‐treated HCC cells. Additionally, knockdown of circ‐SPECC1 inhibited cell proliferation and promoted cell apoptosis of HCC cells under H2O2 treatment. Moreover, circ‐SPECC1 inhibited miR‐33a expression by direct interaction, and miR‐33a inhibitor partially reversed the effect of circ‐SPECC1 knockdown on proliferation and apoptosis of H2O2‐treated HCC cells. Furthermore, TGFβ2 was demonstrated to be a target gene of miR‐33a and TGFβ2 overexpression rescued the phenotypes of HCC cells attenuated by miR‐33a mimics. Meanwhile, autophagy inhibition by 3‐methyladenine (3‐MA) abrogated the effect of miR‐33a mimics on proliferation and apoptosis of H2O2‐treated HCC cells. Finally, knockdown of circ‐SPECC1 hindered tumor growth in vivo. In conclusion, our study demonstrated that circ‐SPECC1 regulated TGFβ2 and autophagy to promote HCC tumorigenesis under oxidative stress via miR‐33a. These findings might provide potential treatment strategies for patients with HCC. |
| first_indexed | 2024-03-08T22:20:29Z |
| format | Article |
| id | doaj.art-a05efc03dabb4e6fad4ee98030db0d9b |
| institution | Directory Open Access Journal |
| issn | 2045-7634 |
| language | English |
| last_indexed | 2024-03-08T22:20:29Z |
| publishDate | 2020-08-01 |
| publisher | Wiley |
| record_format | Article |
| series | Cancer Medicine |
| spelling | doaj.art-a05efc03dabb4e6fad4ee98030db0d9b2023-12-18T12:56:30ZengWileyCancer Medicine2045-76342020-08-019165999600810.1002/cam4.3219Retracted: Circ‐SPECC1 modulates TGFβ2 and autophagy under oxidative stress by sponging miR‐33a to promote hepatocellular carcinoma tumorigenesisBin Zhang0Zhiyi Liu1Kuan Cao2Wengang Shan3Jin Liu4Quan Wen5Renhao Wang6Institute of Digestive Diseases Xuzhou Medical University Xuzhou Jiangsu ChinaInstitute of Digestive Diseases Xuzhou Medical University Xuzhou Jiangsu ChinaInstitute of Digestive Diseases Xuzhou Medical University Xuzhou Jiangsu ChinaInstitute of Digestive Diseases Xuzhou Medical University Xuzhou Jiangsu ChinaInstitute of Digestive Diseases Xuzhou Medical University Xuzhou Jiangsu ChinaInstitute of Digestive Diseases Xuzhou Medical University Xuzhou Jiangsu ChinaInstitute of Digestive Diseases Xuzhou Medical University Xuzhou Jiangsu ChinaAbstract Circular RNAs (circRNAs) play vital roles in the pathogenesis and development of multiple cancers, including hepatocellular carcinoma (HCC). Nevertheless, the regulatory mechanisms of circ‐SPECC1 in HCC remain poorly understood. In our study, we found that circ‐SPECC1 was apparently downregulated in H2O2‐treated HCC cells. Additionally, knockdown of circ‐SPECC1 inhibited cell proliferation and promoted cell apoptosis of HCC cells under H2O2 treatment. Moreover, circ‐SPECC1 inhibited miR‐33a expression by direct interaction, and miR‐33a inhibitor partially reversed the effect of circ‐SPECC1 knockdown on proliferation and apoptosis of H2O2‐treated HCC cells. Furthermore, TGFβ2 was demonstrated to be a target gene of miR‐33a and TGFβ2 overexpression rescued the phenotypes of HCC cells attenuated by miR‐33a mimics. Meanwhile, autophagy inhibition by 3‐methyladenine (3‐MA) abrogated the effect of miR‐33a mimics on proliferation and apoptosis of H2O2‐treated HCC cells. Finally, knockdown of circ‐SPECC1 hindered tumor growth in vivo. In conclusion, our study demonstrated that circ‐SPECC1 regulated TGFβ2 and autophagy to promote HCC tumorigenesis under oxidative stress via miR‐33a. These findings might provide potential treatment strategies for patients with HCC.https://doi.org/10.1002/cam4.3219autophagycirc‐SPECC1HCCmiR‐33aTGFβ2 |
| spellingShingle | Bin Zhang Zhiyi Liu Kuan Cao Wengang Shan Jin Liu Quan Wen Renhao Wang Retracted: Circ‐SPECC1 modulates TGFβ2 and autophagy under oxidative stress by sponging miR‐33a to promote hepatocellular carcinoma tumorigenesis Cancer Medicine autophagy circ‐SPECC1 HCC miR‐33a TGFβ2 |
| title | Retracted: Circ‐SPECC1 modulates TGFβ2 and autophagy under oxidative stress by sponging miR‐33a to promote hepatocellular carcinoma tumorigenesis |
| title_full | Retracted: Circ‐SPECC1 modulates TGFβ2 and autophagy under oxidative stress by sponging miR‐33a to promote hepatocellular carcinoma tumorigenesis |
| title_fullStr | Retracted: Circ‐SPECC1 modulates TGFβ2 and autophagy under oxidative stress by sponging miR‐33a to promote hepatocellular carcinoma tumorigenesis |
| title_full_unstemmed | Retracted: Circ‐SPECC1 modulates TGFβ2 and autophagy under oxidative stress by sponging miR‐33a to promote hepatocellular carcinoma tumorigenesis |
| title_short | Retracted: Circ‐SPECC1 modulates TGFβ2 and autophagy under oxidative stress by sponging miR‐33a to promote hepatocellular carcinoma tumorigenesis |
| title_sort | retracted circ specc1 modulates tgfβ2 and autophagy under oxidative stress by sponging mir 33a to promote hepatocellular carcinoma tumorigenesis |
| topic | autophagy circ‐SPECC1 HCC miR‐33a TGFβ2 |
| url | https://doi.org/10.1002/cam4.3219 |
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