As the most common primary liver cancer, hepatocellular carcinoma (HCC) is the sixth leading cause of cancer-related mortality worldwide, with an estimated 750 000 new deaths annually. 1 Although therapeutic strategies of HCC have been improved greatly, HCC is still notorious for its poor prognosis, metastasis and recurrence. 2 Therefore, novel therapeutic strategies and potential biomarkers focusing on the molecular mechanism of hepatocarcinogenesis are of great significance. Widely found in eukaryotes, circular RNAs (circRNAs) are a subclass of endogenous non-coding RNAs bearing a closed covalent loop. 3 It has been proved that circRNAs are mainly conserved in the cytoplasm, and they are stable and not easily degraded by RNA exonuclease. 4 In recent years, increasing studies have shown that circRNAs participate in various biological processes, including acting as miRNA sponge, and regulating protein binding and gene transcription. 5,6 Notably, the role of circRNAs in multiple cancers may show their potential as diagnostic biomarkers. 7 For example, circCCDC9

Background/Aim. Curcumin exhibits anticancer effects against various types of cancer including hepatocellular carcinoma (HCC). miR-21 has been reported to be involved in the malignant biological properties of HCC. However, whether miR-21 plays a role in curcumin-mediated treatment of HCC is unknown. The purpose of this study was to identify the potential functions and mechanisms of miR-21 in curcumin-mediated treatment of HCC. Methods. The anticancer effects of curcumin were assessed in vivo and in vitro. The underlying mechanism of miR-21 in curcumin-mediated treatment of HCC was assessed by quantitative real-time PCR (RT-qPCR), western blot, and Dual-Luciferase Reporter assays. Results. The present study revealed that curcumin suppressed HCC growth in vivo and inhibited HCC cell proliferation and induced cell apoptosis in a dose-dependent manner in vitro. Meanwhile, the curcumin treatment can downregulate miR-21 expression, upregulate TIMP3 expression, and inhibit the TGF-β1/smad3 signaling pathway. miR-21 inhibition enhanced the effect of curcumin on cell proliferation inhibition, apoptosis, and TGF-β1/smad3 signaling pathway inhibition in HepG2 and HCCLM3 cells. It demonstrated that TIMP3 was a direct target gene of miR-21. Interestingly, the effect of miR-21 inhibition on cell proliferation, apoptosis, and TGF-β1/smad3 signaling pathway in HepG2 and HCCLM3 cells exposed to curcumin was attenuated by TIMP3 silencing. Conclusion. Taken together, the present study suggests that miR-21 is involved in the anticancer activities of curcumin through targeting TIMP3, and the mechanism possibly refers to the inhibition of TGF-β1/smad3 signaling pathway.

BackgroundHepatocellular carcinoma (HCC) is one of the most common types of cancer that is associated with poor quality of life in patients and a global health burden. The mechanisms involved in the development and progression of HCC remain poorly understood.MethodsHepatocellular carcinoma human samples and cell lines were subjected to qRT-PCR for expression assessment. CCK-8 assay, Transwell migration and invasion assay, were applied for cell function detection. Animal experiment was used to measure the function of SNHG17 on cell growth in vivo. Western blot was conducted to evaluate the level of EMT in cells. RIP, RNA pull-down and luciferase reporter assays were performed to assess the correlation between SNHG17, miR-3180-3p and RFX1.ResultsOur study demonstrated that SNHG17 was upregulated in HCC human samples and involved cell proliferation, migration, invasion progress. SNHG17 promoted HCC cell growth and metastasis in vivo. Furthermore, we investigated the downstream factor of SNHG17, SNHG17 acted as a molecular sponge for miR-3180-3p, and SNHG17 regulated RFX1 expression via miR-3180-3p. SNHG17 promotes tumor-like behavior in HCC cells via miR-3180-3p/RFX1.ConclusionWe determined RFX1 as the target of miR-3810-3p; SNHG17 enhanced the progression of HCC via the miR-3180-3p/RFX1 axis. Taken together, our findings may provide insight into the molecular mechanism involved in the progression of HCC and develop SNHG17 as a novel therapeutic target against HCC.

Background: The relationship between vitamin D and non-alcoholic fatty liver disease (NAFLD) has been a subject of significant interest. This study aimed to assess the current research status of vitamin D and NAFLD through a systematic analysis using bibliometric methods. Methods: A search of the Web of Science Core Collection database was conducted to identify relevant literature meeting the study criteria. Key information such as the number of publications, authors, countries, and keywords was extracted. Results: A total of 416 articles were included for analysis. The findings revealed an increasing trend in research on vitamin D and NAFLD in recent years. The dominant forces in the field were concentrated in China and the United States. A few institutions contributed to the majority of the research output, and the research topics primarily covered the association between vitamin D and NAFLD in terms of disease risk, severity, and treatment efficacy. Conclusion: The bibliometric analysis of the literature in this study provided insights into the current status and trends of research on vitamin D and NAFLD. These findings are of significant importance in guiding future research directions and collaborations, offering new perspectives and strategies for the prevention and treatment of NAFLD. Further research should delve into the mechanisms underlying the association between vitamin D and NAFLD, and more clinical trials should be conducted to evaluate the potential role of vitamin D in the treatment of NAFLD.