Cancer is the second leading cause of death after cardiovascular disease. In 2015, >8.7 million people died worldwide due to cancer, and by 2030 this figure is expected to increase to ~13.1 million. Tumor chemotherapy drugs have specific toxicity and side effects, and patients can also develop secondary drug resistance. To prevent and treat cancer, scientists have developed novel drugs with improved antitumor effects and decreased toxicity. Ailanthone (AIL) is a quassinoid extract from the traditional Chinese medicine plant Ailanthus altissima , which is known to have anti-inflammatory and antimalarial effects. An increasing number of studies have focused on AIL due to its antitumor activity. AIL can inhibit cell proliferation and induce apoptosis by up- or downregulating cancer-associated molecules, which ultimately leads to cancer cell death. Antitumor effects of AIL have been observed in melanoma, acute myeloid leukemia, bladder, lung, breast, gastric and prostate cancer and vestibular neurilemmoma. To the best of our knowledge, the present study is the first review to describe the antitumor mechanisms of AIL.
Gastrointestinal stromal tumors (GISTs) are the most commonly observed mesenchymal tumors of the digestive tract, and they originate from the interstitial cells of Cajal. GISTs can be divided into KIT/PDGFRA-mutant GISTs and wild-type GISTs based on the presence or absence of KIT/PDGFRA mutations. Wild-type GISTs can be divided into succinate dehydrogenase complex (SDH)-deficient GISTs and non-SDH-deficient GISTs. Downstream signaling pathways activated by these mutations serve a pivotal role in the development of GISTs and are associated with the biological behavior, including risk stratification, clinical prognosis and drug resistance. Accurate medical care requires accurate molecular diagnosis, which in turn prolongs the survival of patients with GISTs and makes GIST a chronic disease. At present, there is a lack of effective treatment for imatinib/sunitinib/regorafenib resistant patients and KIT/PDGFRA-WT GISTs, which is undoubtedly a major challenge for future research. The present review summarizes the molecular pathogenesis of GISTs and the progress of related research.
Background Chronic liver disease poses an escalating health challenge on a global scale. It has been suggested that prolonged exposure to heavy metals could potentially contribute to the development of non-alcoholic fatty liver disease (NAFLD). Our study aimed to assess the correlation between urinary levels of specific heavy metals, including Ba, Cd, Co, Cs, Hg, Mo, Pb, Sb, Sn, Ti, and Ur, and the occurrence of NAFLD and advanced liver fibrosis within the general population of the United States. Methods In our study, we conducted a thorough analysis using data from the NHANES spanning from 2013 to 2018. To examine the correlation between urinary heavy metal concentration and the prevalence of NAFLD and advanced liver fibrosis, we employed a multivariable analysis that accounted for various factors such as sociodemographic characteristics, lifestyle factors, hypertension, and T2DM. This allowed us to control for potential confounding variables and obtain reliable findings regarding the association between urinary heavy metal concentration and the occurrence of NAFLD and advanced liver fibrosis. Results We employed multiple logistic regression models to examine the data, and the results revealed noteworthy findings. Higher levels of urinary Ba, Cd, Co, Pb, Sb, Sn, Tu, and Ur exhibited a significant positive association with NAFLD. Additionally, as the concentration of Cd, Pb, Sb, and Sn increased in urine, the likelihood of advanced liver fibrosis also significantly increased. These findings underscore the significant positive associations between the levels of specific heavy metals in urine and both NAFLD and advanced liver fibrosis. Conclusion The findings of this study suggest a significant association between elevated urinary Ba, Cd, Co, Pb, Sb, Sn, Tu, Ur concentration and NAFLD while a significant correlation was also found between higher urinary levels of Cd, Pb, Sb, Sn and advanced liver fibrosis.
Gastric cancer is the third leading cause of cancer-related deaths worldwide, and research on gastric cancer pathogenesis is fundamental. Long intergenic non-coding RNAs (lincRNAs) control cancer initiation and progression through several mechanisms, with the competitive endogenous RNA (ceRNA) regulatory network being the most common. In this study, in situ hybridization revealed that long intergenic non-protein coding RNA-regulator of reprogramming (linc-ROR) was highly expressed in gastric cancer cells and was mainly cytoplasmic-positive. Cell counting kit-8 (CCK-8), plate colony formation, wound healing, and Transwell assay revealed that linc-ROR knockdown impedes the growth, proliferation, and migration of gastric cancer cells, while linc-ROR overexpression promoted gastric cancer cell growth, migration, and colony formation ability. Combined with previous studies, the molecular mechanism axis of linc-ROR /miR-145-5-5p/ POU5F1/ SOX2 was verified. The expression of linc-ROR knockdown significantly suppressed the protein expression of POU5F1 and SOX2. Co-transfection with linc-ROR siRNA reverses the carcinogenic effect of the miR-145-5p inhibitor on gastric cancer cell proliferation, cloning, and migration. These findings lay a foundation for developing novel targets for gastric cancer treatment.
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