Objective The study aims to elucidate the inhibitory effects of curcumin on the proliferation of colon cancer RKO cells,focusing on the regulatory mechanisms of tripartite motif-containing protein 2(TRIM2)expression and the mammalian target of rapamycin(mTOR)signaling pathway.Methods Experimental concentrations of curcumin were determined by calculating the half maximal inhibitory concentration(IC50)value.Quantitative polymerase chain reaction(qPCR)was utilized to assess the level of TRIM2 expression in RKO and fetal human colon(FHC)cells.Western blotting analysis was conducted to investigate the level of TRIM2 expression and mTOR pathway-related proteins in curcumin-treated RKO cells.The impact of curcumin treatment,TRIM2-knockingdown,and mTOR signaling pathway on proliferation in RKO cells was quantified using the cell counting kit-8(CCK8)assay.Results The expression of TRIM2 was found to be elevated in RKO cells as determined by qPCR,compared to FHC cells.Curcumin suppressed the level of TRIM2 expression,and subsequent knockdown of TRIM2 resulted in decreased expression of mTOR-related proteins in RKO cells.Both curcumin and TRIM2-knockdown demonstrated significant inhibition of proliferation in RKO cells,with reversion upon activation of mTOR signaling pathway.Conclusion The study unveils the inhibitory effects of curcumin on RKO cells proliferation through modulation of TRIM2 expression and the mTOR signaling pathway.

Objective The study aims to elucidate the inhibitory effects of curcumin on the proliferation of colon cancer RKO cells,focusing on the regulatory mechanisms of tripartite motif-containing protein 2(TRIM2)expression and the mammalian target of rapamycin(mTOR)signaling pathway.Methods Experimental concentrations of curcumin were determined by calculating the half maximal inhibitory concentration(IC50)value.Quantitative polymerase chain reaction(qPCR)was utilized to assess the level of TRIM2 expression in RKO and fetal human colon(FHC)cells.Western blotting analysis was conducted to investigate the level of TRIM2 expression and mTOR pathway-related proteins in curcumin-treated RKO cells.The impact of curcumin treatment,TRIM2-knockingdown,and mTOR signaling pathway on proliferation in RKO cells was quantified using the cell counting kit-8(CCK8)assay.Results The expression of TRIM2 was found to be elevated in RKO cells as determined by qPCR,compared to FHC cells.Curcumin suppressed the level of TRIM2 expression,and subsequent knockdown of TRIM2 resulted in decreased expression of mTOR-related proteins in RKO cells.Both curcumin and TRIM2-knockdown demonstrated significant inhibition of proliferation in RKO cells,with reversion upon activation of mTOR signaling pathway.Conclusion The study unveils the inhibitory effects of curcumin on RKO cells proliferation through modulation of TRIM2 expression and the mTOR signaling pathway.

OBJECTIVE: To investigate the effect of lncRNA-CASC2 (CASC2) /miR-155-5p/APC axis to the progression of non-Hodgikn lymphoma (NHL). METHODS: The expression level of CASC2 and miR-155-5p in NHL cell lines were examined by qRT-PCR. Dual-luciferase reporter gene assay was used to verify the relationship between miR-155-5p, CASC2 and APC. The effects of CASC/miR-155-5p/APC axis to the proliferation, invasion and apoptosis of NK-92 cells were detected by MTT, Transwell assay and flow cytometry assay, respectively. RESULTS: CASC2 was downregulated in NHL cell lines. Overexpression of CASC2 could inhibit the proliferation and invasion of NK-92 cells, and promote its apoptosis. Dual-luciferase reporter gene assay confirmed that there was a targeting relationship between miR-155-5p, CASC2 and APC. The restoration experiments proved that knockdown of both miR-155-5p and CASC2 or APC could restore the inhibitory effect of miR-155-5p silencing to the biological behavior of NK-92 cells. CONCLUSION Overexpression of CASC2 suppresses the proliferation and invasion of NK-92 cells, promote the apoptosis of NK-92 cells via targeting miR-155-5p and upregulating APC expression.
Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Humans ; Lymphoma, Non-Hodgkin/genetics* ; MicroRNAs/genetics* ; RNA, Long Noncoding/genetics* ; Tumor Suppressor Proteins/genetics*

Objective To evaluate the clinical efficacy of pingyangmycin (PYM) injection on infantile hemangioma located in the parotid gland region. Methods Twelve patients were treated by intralesional injection of PYM. When necessary, the injections were repeated at an interval of one week, but not more than 3-4 sessions within a therapeutic period. Normally, the secondary therapeutic period was performed 1 month later. The general and local adverse responses were recorded and the clinical outcomes were assessed with a follow-up of 1 to 3 years. Results Complete clinical resolutions were achieved in 10 patients. 2 patients received one injection, 3 patients received 2 injections, 3 patients received 3 injections, and 2 patients received 4 injections. The remaining 2 patients with partial resolution received 6 and 7 injections respectively. No clinical recurrence was observed during the follow-up of 1 to 3 years. No ulcerations or postoperative sears in injection regions were presented. The function of facial nerve was remained normality in all patients. The systematic side effects included transient pyrexia and poor appetite appeared in partial patients. No allergy cases were found. Conclusion Treatment of infantile hemangioma located in parotid gland region with PYM injection reveals a high rate of complete clinical resolution, with fair cosmetic results and short treatment time, and it does not damage the facial nerve or form local scar.The treatment time of PYM injection seems to be positively related to size of the lesions.