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Abstract Background The Cdc42-interacting protein-4, Trip10 (also known as CIP4), is a multi-domain adaptor protein involved in diverse cellular processes, which functions in a tissue-specific and cell lineage-specific manner. We previously found that Trip10 is highly expressed in estrogen receptor-expressing (ER+) breast cancer cells. Estrogen receptor depletion reduced Trip10 expression by progressively increasing DNA methylation. We hypothesized that Trip10 functions as a tumor suppressor and may be involved in the malignancy of ER-negative (ER-) breast cancer. To test this hypothesis and evaluate whether Trip10 is epigenetically regulated by DNA methylation in other cancers, we evaluated DNA methylation of Trip10 in liver cancer, brain tumor, ovarian cancer, and breast cancer. Methods We applied methylation-specific polymerase chain reaction and bisulfite sequencing to determine the DNA methylation of Trip10 in various cancer cell lines and tumor specimens. We also overexpressed Trip10 to observe its effect on colony formation and in vivo tumorigenesis. Results We found that Trip10 is hypermethylated in brain tumor and breast cancer, but hypomethylated in liver cancer. Overexpressed Trip10 was associated with endogenous Cdc42 and huntingtin in IMR-32 brain tumor cells and CP70 ovarian cancer cells. However, overexpression of Trip10 promoted colony formation in IMR-32 cells and tumorigenesis in mice inoculated with IMR-32 cells, whereas overexpressed Trip10 substantially suppressed colony formation in CP70 cells and tumorigenesis in mice inoculated with CP70 cells. Conclusions Trip10 regulates cancer cell growth and death in a cancer type-specific manner. Differential DNA methylation of Trip10 can either promote cell survival or cell death in a cell type-dependent manner.

Background Numerous studies have examined the clinical effectiveness of transforaminal full endoscopic lumbar diskectomy (T-FELD) and interlaminar full endoscopic lumbar diskectomy (I-FELD) for L5–S1 lumbar disk herniation (LDH), with mixed findings. The goal of this systematic review and meta-analysis was to evaluate the perioperative outcomes, clinical results, and complications of T-FELD and I-FELD to determine their efficacy and safety for treating L5–S1 LDH and to examine the features of complications in depth. Methods Several databases were searched for articles that matched all of the inclusion criteria. The visual analog scale (VAS) and Oswestry Disability Index (ODI) were used to assess the clinical results. Information on perioperative outcomes and complications was gathered and analyzed. Results Eight studies with 756 participants were included. There were no significant differences in postoperative bed time (p = 0.44) and hospitalization time (p = 0.49) between T-FELD and I-FELD. When compared with I-FELD, T-FELD was associated with substantially longer fluoroscopy time (p < 0.0001) and operating time (p < 0.0001). There were no significant differences in the preoperative and postoperative VAS and ODI scores between T-FELD and I-FELD. The rates for overall complications, postoperative dysesthesia, postoperative lower extremity pain, incomplete decompression, recurrence, and conversion to open surgery were comparable for T-FLED and I-FELD. Conclusion T-FELD and I-FELD had equal clinical results and safety for treatment of L5–S1 LDH. Fluoroscopy and operative times were shorter for I-FELD than for T-FELD. [ABSTRACT FROM AUTHOR]

Osteosarcoma is a malignant bone tumor affecting adolescents and children. No effective treatment is currently available. Asiatic acid (AA), a triterpenoid compound found in Centella asiatica, possesses anti‐tumor, anti‐inflammatory, and anti‐oxidant properties in various types of tumor cells. This study aims to determine whether AA exerts antitumor effects in human osteosarcoma cells. Our results indicate that AA does not influence the viability, proliferative rate, or cell cycle phase of human osteosarcoma cells under non‐toxic conditions. AA suppressed osteosarcoma cell migration and invasion by down‐regulating matrix metalloproteinase 1 (MMP1) expression. Data in the TNMplot database suggested MMP1 expression was higher in osteosarcoma than in normal tissues, with associated clinical significance observed in osteosarcoma patients. Overexpression of MMP1 in osteosarcoma cells reversed the AA‐induced suppression of cell migration and invasion. AA treatment decreased the expression of specificity protein 1 (Sp1), while Sp1 overexpression abolished the effect of AA on MMP1 expression and cell migration and invasion. AA inhibited AKT phosphorylation, and treatment with a PI3K inhibitor (wortmannin) increased the anti‐invasive effect of AA on osteosarcoma cells via the p‐AKT/Sp1/MMP1 axis. Thus, AA exhibits the potential for use as an anticancer drug against human osteosarcoma. [ABSTRACT FROM AUTHOR]