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Mar 2024 DOI 10.14302/issn.2997-2108.jcc-23-4838
Among the reproductive cancers cervical cancer has special place, because the second most frequent cause of cancer-related death among women worldwide. The studies suggested that the PI3K/mTOR/AKT signaling pathway is associated with certain reproductive tumors. A lot of research is ongoing for understanding this pathway evidence of its role in promoting tumorigenesis and recent progress in the development of therapeutic agents that targeted PI3K/AKT. In this a single-arm study included 34 Azerbaijan population woman with HPV-negative cervical tumors. The core genes of PAM signaling pathway were analyzed using RT-PCR method. Our preliminary results suggested that tumorgenesis of HPV-negative cervical cancer patients approximately 25% associated with dysregulation of PAM signaling pathway reason which are core genes alteration. The overall survival times in the PAM-active and PAM-stable patients were not significantly varies. However, the main factor for overall survival times were treatment strategy: both PAM-active and PAM-stable patients who received radiation therapy alone had a shorter overall survival than patients who received radiation plus chemotherapy. The patients with alteration of ATK1 and mTOR genes in PAM signaling pathway had poor prognosis then patients with PIK3CA and PTEN mutation
Jan 2021 DOI 10.14302/issn.2470-5020.jnrt-20-3619
Circular RNAs (circRNAs) are recently rediscovered eukaryotic molecules that form a covalently closed-loop structure through a special type of alternative splicing known as backsplicing. These closed-loop structures are highly stable and resistant to RNase degradation, and are thereby expressed in a tissue-specific and evolutionarily conserved manner, which regulates the expression of proteins and mRNAs that are involved in the metabolic pathways associated with specific diseases. Recent evidence of the ubiquitous expression of circRNAs in cancer under physiological and pathophysiological conditions indicates that dysregulation of gene and protein expression might promote tumorigenesis and carcinogenesis, and that circRNAs have important clinical significance in the diagnosis, treatment, and prognosis of cancer and other diseases. This review provides a brief introduction to the characteristics, formation, and function of circRNAs. Some of circRNAs act as microRNA (miRNA) sponges to regulate the level of transcriptional splicing and the expression of parental genes through the circRNA-miRNA-mRNA regulation axis. We summarize recent progress in above-mentioned circRNAs associated with Alzheimer's disease (AD).
Mar 2018 DOI 10.14302/issn.2639-1716.jn-18-1993
Cardiovascular disease and lung cancer are two of the most common causes of death in the United States. The cardioprotective benefits of statin class drugs is predominantly mediated through the inhibition of 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase, decreasing available mevalonate, and thus limiting in vivo cholesterol biosynthesis. Mevalonate and its metabolites have significant roles in cellular membrane synthesis, which is dysregulated during tumorigenesis, and is therefore a potential source for anti-tumor effects of statins. Similarly, dysregulation of cellular signaling is a hallmark of tumorigenesis. In vitro studies of EGFR, RAS, and AKT signaling pathways in cancer cells can all be reformed back to states more indicative of normally functioning cells when treated with statins. Statins have also been shown to exert beneficial properties in the presence of chemotherapeutic medications and radiation therapies by modulating the deleterious effects of reactive oxygen species, decreasing tumor cell resistance, and minimizing damage to surrounding native tissues. There is abundant of in vitro evidence to support the beneficial effects of statins on lung cancer patients. Prospective studies to determine the value of statin therapy on lung cancer prevention could lead to a significant change in lung cancer treatment.
Jul 2017 DOI 10.14302/issn.2639-1716.jn-17-1495
Diets high in unsaturated fatty acids, especially those containing high levels of linoleic acid, e.g., corn oil, enhance mammary gland tumorigenesis in experimental animals. In contrast, diets high in long-chain polyunsaturated fatty acids such as eicosapentaenoic (EPA) and docosahexaenoic (DHA), e.g. menhaden oil, appear to have a suppressive effect on this tumorigenic process. Many mechanisms have been proposed to explain the tumor inhibitory action exerted by menhaden oil and other fish oils, e.g., differences in prostaglandin metabolism, energy efficiency, alterations of the immune system, changes in lipid peroxidation, etc. Fundamental to a mechanistic understanding of this phenomenon, however, is an understanding as to whether or not the tumor inhibitory activities of dietary fish oil is mediated via an inhibition of tumor cell proliferation or mediated via an enhancement of tumor cell loss. Whether the amount of dietary fat or the type of fat effects mammary tumorigenic processes, via an effect on tumor cell proliferation or tumor cell loss, has not been clearly established. In the studies described in this communication, three methods were utilized to study tumor cell proliferation, i.e., H3-thymidine autoradiographic analysis, 5-bromo 2'-deoxyuridine (Brdu) flow cytometric analysis, and proliferative cell nuclear antigen (PCNA) flow cytometric analysis. Two methods were used to study tumor cell loss, i.e., a determination of the I125Urd tumor emission rate and a determination of a cell loss factor from the formulas of Steel and Begg. The tumor examined was the human breast carcinoma cell line MDA- MB231 maintained in athymic nude mouse. No significant difference in cell proliferation between carcinomas of mice fed a high corn oil diet (20% w/w) and a diet high in fish oil (19% menhaden oil, 1% corn oil). In contrast, a significant (p<0.05) increase in the rate of I125Urd emission rate and cell loss factor from the carcinomas in the fish oil fed mice compared to the corn oil fed mice was observed. In summary, the decreased tumor volume in the human breast carcinomas maintained in athymic nude mice fed a fish oil diet as compared to those fed a corn oil diet, appears to be due, at least in part, to an increased rate of carcinoma cell loss rather than a decreased rate of carcinoma cell proliferation.
Jun 2016 DOI 10.14302/issn.2372-6601.jhor-16-1125
Senescence is a powerful mechanism that prevents the development of tumors in vivo; however, once tumors are formed, most are refractory to senescence in response to oncogenic stress. Therefore, a novel pathway leading to senescence is required. We herein demonstrated that the cell cycle regulator CDC6 translocated from the nucleus to the cytoplasm during senescence in a leptomycin B-resistant manner. In order to evaluate the translocation of CDC6, we utilized an estrogen receptor (ER) tag to retain CDC6 in the cytoplasm. ER-tagged CDC6 was exclusively cytoplasmic, inhibited cell proliferation, and induced senescence-associated (SA) b-galactosidase activity. Furthermore, ER-CDC6 inhibited the transformation of mouse fibroblasts by the active ras oncogene in vitro, and suppressed tumor formation in NOD-SCID mice. Thus, CDC6 may play a critical role in the regulation of senescence in the cytoplasm in order to counteract tumorigenesis.