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Na Yan,1 Xianggui Wang,1 Zufang Xu,1 Linling Zhong,1 Jiangyong Yang2 1Department of Vasculocardiology, Ganzhou People’s Hospital, Ganzhou, People’s Republic of China; 2Department of Cardiology, Ganzhou Hospital of Guangdong Provincial People’s Hospital, Ganzhou Municipal Hospital, Ganzhou, People’s Republic of ChinaCorrespondence: Jiangyong Yang, Department of Cardiology, Ganzhou Hospital of Guangdong Provincial People’s Hospital, Ganzhou Municipal Hospital, No. 49, Dagong Road, Ganzhou, 341000, People’s Republic of China, Tel +86-797-8208553, Email yangjy19861208@163.comIntroduction: Apigenin is a natural flavonoid compound with promising potential for the attenuation of myocardial hypertrophy (MH). The compound can also modulate the expression of miR-185-5p that both promote MH and suppress autophagy. The current attempts to explain the anti-MH effect of apigenin by focusing on changes in miR-185-5p-mediated autophagy.Methods: Hypertrophic symptoms were induced in rats using transverse aortic constriction (TAC) method and in cardiomyocytes using Ang II and then handled with apigenin. Changes in myocardial function and structure and cell viability and surface area were measured. The role of miR-185-5p in the anti-MH function of apigenin was explored by detecting changes in autophagic processes and miR-185-5p/SREBP2 axis.Results: TAC surgery induced weight increase, structure destruction, and collagen deposition in hearts of model rats. Ang II suppresses cardiomyocyte viability and increased cell surface area. All these impairments were attenuated by apigenin and were associated with the restored level of autophagy. At the molecular level, the expression of miR-185-5p was up-regulated by TAC, while the expression of SREBP2 was down-regulated, which was reserved by apigenin both in vivo and in vitro. The induction of miR-185-5p in cardiomyocytes could counteracted the protective effects of apigenin.Discussion: Collectively, the findings outlined in the current study highlighted that apigenin showed anti-MH effects. The effects were related to the inhibition of miR-185-5p and activation of SREBP, which contributed to the increased autophagy.Keywords: apigenin, autophagy, miR-185-5p, myocardial hypertrophy, SREBP2

Istianah Purnamasari, Yuyun Sri Wahyuni, Hernawati Basir Department of Pharmacy, Faculty of Medicine and Health Science, Universitas Muhammadiyah Makassar, Makassar, South Sulawesi, IndonesiaCorrespondence: Istianah Purnamasari, Department of Pharmacy, Faculty of Medicine and Health Science, Universitas Muhammadiyah Makassar, Makassar, South Sulawesi, Indonesia, Email istianahpurnamasari@unismuh.ac.id

Background: Long non-coding RNAs (lncRNAs) have been reported to play essential roles in regulating the radiosensitivity of cancers. Prostate cancer-associated transcript 6 ( PCAT6 ) exerts oncogenic roles in several tumors. However, the roles of PCAT6 and its underlying mechanism in regulating the radiosensitivity of triple-negative breast cancer (TNBC) have not been investigated., Methods: The expression levels of PCAT6, microRNA-185-5p ( miR-185-5p ) and tumor protein D52 ( TPD52 ) were determined by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability, apoptosis and colony formation were assessed by Cell Counting Kit-8 (CCK-8) assay, flow cytometry and colony formation assay, respectively. The interaction between miR-185-5p and PCAT6 or TPD52 was predicted by bioinformatics analysis and verified by dual-luciferase reporter assay. Western blot was carried out to detect the protein level of TPD52., Results: PCAT6 and TPD52 were highly expressed and miR-185-5p was lowly expressed in TNBC tissues and cells, which was associated with an aggressive tumor phenotype in patients, affecting lymph node metastasis and clinical stage. PCAT6 or TPD52 knockdown or miR-185-5p overexpression enhanced the radiosensitivity of TNBC cells via inhibiting proliferation and inducing apoptosis. PCAT6 directly interacted with miR-185-5p and negatively regulated miR-185-5p expression. Moreover, TPD52 was confirmed as a target of miR-185-5p . Besides, PCAT6 regulated the radiosensitivity of TNBC cells through acting as a molecular sponge of miR-185-5p to modulate TPD52 expression., Conclusion: Knockdown of PCAT6 promoted the radiosensitivity of TNBC cells through regulating miR-185-5p / TPD52 axis, providing a vital theoretical basis to improve the radiotherapy efficiency of TNBC., Competing Interests: The authors report no funding and no conflicts of interest in this work., (© 2020 Shi et al.)