Use of TCAM was highly prevalent among children with cancer residing in Guatemala. Most importantly, TCAM was used alongside conventional therapy for supportive care indications. These findings underscoring the need for open lines of communication between clinicians and families. Future research may consider exploring the role of TCAM within the scope of supportive care and its effect on existing supportive care interventions.
Background: To investigate the effects of taurine on prostate cancer cell proliferation and apoptosis, and on the mammalian sterilization of a 20-like kinase-1 (MST1)/Hippo signaling pathway. Methods:The prostate cancer DU145 cell line was selected and the 3-(4,5-dimethylthiazol-2-yl)-2,5diphenyltetrazolium bromide (MTT) method was used to determine the rate of inhibition by taurine on the proliferation of the cells at 1, 10 −1 , 10 −2 , 10 −3 , 10 −4 , 10 −5 and 10 −6 mg/mL to obtain the taurine intervention concentrations. The cultured cells were divided into three groups: the blank group was cultured with conventional culture medium, the positive control group was cultured with 2 mg/mL cisplatin, and the taurine group was cultured with the determined taurine intervention concentrations of 0.003 mg/mL as low, 0.03 mg/mL as medium and 0.3 mg/mL as high concentration. After 72 h incubation, cell proliferation, apoptosis and cellular MST1/Hippo signaling pathway protein expression were observed.Results: In the comparison of cell proliferation rate, the taurine group was lower than the positive control group and the blank group (P<0.05), the cell proliferation rate of different concentrations in the taurine group decreased with the increase of concentration (P<0.05). The apoptosis rate was higher in the taurine group than in the positive control group and the blank group (P<0.05), the apoptosis rate increased with increasing concentration in the taurine group (P<0.05). The expression of MST1 and Bax was higher in the taurine group than in the positive control group and the blank group (P<0.05), the expression of MST1 and Bax increased with increasing concentration in the taurine group (P<0.05). The expression of YAP and Bcl-2 was lower in the taurine group than in the positive control group and the blank group (P<0.05), the expression of YAP and Bcl-2 decreased with increasing concentration in the taurine group (P<0.05).Conclusions: Taurine promoted apoptosis and inhibited proliferation of prostate cancer cells, and its mechanism of action may be related to the MST1/Hippo signaling pathway in a dose-dependent manner.
Emerging articles have reported that N6-methyladenosine (m6A) modification is mainly involved in clear-cell renal cell carcinoma (ccRCC) tumorigenesis. However, the regulatory mechanisms of m6A reader IGF2BP1 involved in ccRCC tumor energy metabolism are currently unknown. Results showed that the m6A reader IGF2BP1 exhibited significantly higher expression in ccRCC cells. Functionally, results by gain/loss functional assays indicated that IGF2BP1 promoted the glycolytic characteristics, including glucose uptake, lactate production and extracellular acidification rate (ECAR). Mechanistically, IGF2BP1 recognized the m6A modified sites on LDHA mRNA and enhanced its mRNA stability, thereby accelerating tumor energy metabolism. Thus, our work reveals a novel facet of the m6A that promoted mRNA stability and highlighted the functional importance of IGF2BP1 as m6A readers in post-transcriptional gene regulation.
Objective. This study is aimed at exploring the effect of Qinghua Jianpi Recipe on preventing colon polyp recurrence and inhibiting the progress of “inflammatory cancer transformation.” And another goal is to explore the changes of intestinal flora structure and intestinal inflammatory (immune) microenvironment of mice with colon polyps treated by Qinghua Jianpi Recipe and to clarify its mechanism. Methods. Clinical trials were conducted to confirm the therapeutic effect of Qinghua Jianpi Recipe on patients with inflammatory bowel disease. The inhibitory effect of Qinghua Jianpi Recipe on “inflammatory cancer transformation” of colon cancer was confirmed by an adenoma canceration mouse model. Histopathological examination was used to evaluate the effects of Qinghua Jianpi Recipe on intestinal inflammatory state, adenoma number, and pathological changes of adenoma model mice. The changes of inflammatory indexes in intestinal tissue were tested by ELISA. Intestinal flora was detected by 16S rRNA high-throughput sequencing. Short-chain fatty acid metabolism in the intestine was analyzed by targeted metabolomics. Network pharmacology analysis of possible mechanism of Qinghua Jianpi Recipe on colorectal cancer was performed. Western blot was used to detect the protein expression of the related signaling pathways. Results. Qinghua Jianpi Recipe can significantly improve intestinal inflammation status and function in patients with inflammatory bowel disease. Qinghua Jianpi Recipe could significantly improve the intestinal inflammatory activity and pathological damage of adenoma model mice and reduce the number of adenoma. Qinghua Jianpi Recipe significantly increased the levels of Peptostreptococcales_Tissierellales, NK4A214_group, Romboutsia, and other intestinal flora after intervention. Meanwhile, the treatment group of Qinghua Jianpi Recipe could reverse the changes of short-chain fatty acids. Network pharmacology analysis and experimental studies showed that Qinghua Jianpi Recipe inhibited the “inflammatory cancer transformation” of colon cancer by regulating intestinal barrier function-related proteins, inflammatory and immune-related signaling pathways, and free fatty acid receptor 2 (FFAR2). Conclusion. Qinghua Jianpi Recipe can improve the intestinal inflammatory activity and pathological damage of patient and adenoma cancer model mice. And its mechanism is related to the regulation of intestinal flora structure and abundance, short-chain fatty acid metabolism, intestinal barrier function, and inflammatory pathways.
It has been reported that N6-methyladenosine (m6A) modification is mainly involved in clear-cell renal cell carcinoma (ccRCC) tumorigenesis. However, the regulatory mechanisms of m6A reader IGF2BP1 involved in ccRCC tumor energy metabolism are currently unknown. Results showed that the m6A reader IGF2BP1 exhibited significantly higher expression in ccRCC cells. Functionally, results by gainloss functional assay indicated that IGF2BP1 promoted the glucolytic characteristics, including glucose uptake, lactate production and extracellular acidification rate (ECAR). Mechanistically, IGF2BP1 recognizes the m6A modified sites on LDHA mRNA and enhances its mRNA stability, thereby accelerating tumor energy metabolism. Thus, our work reveals a novel facet of the m6A that promotes mRNA stability and highlights the functional importance of IGF2BP1 as m6A readers in post-transcriptional gene regulation.
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