Уважаемые коллеги, доброго времени суток! Представляем вам швейцарское научное издание Frontiers in Molecular Biosciences. Журнал имеет первый квартиль, находится в открытом доступе, издается в Frontiers Media S.A., его SJR за 2019 г. импакт-фактор - 4,188, равен 1,808, электронный ISSN - 2296-889X, предметные области - Общие вопросы биохимии, генетики и молекулярной биологии, Биохимия, Молекулярная биология. Вот так выглядит обложка:
Редактором является Анналиса Пасторе, контактные данные - annalisa.1.pastore@kcl.ac.uk, editorial.office@frontiersin.org, support@frontiersin.org, institutions@frontiersin.org
Большая часть современных исследований в области естественных наук посвящена молекулярному пониманию взаимосвязей между генами и окружающей средой, в частности, динамическим изменениям уровней, модификаций и взаимодействий клеточных эффекторов, включая белки. Frontiers in Molecular Biosciences является международной публикационной платформой для фундаментальных и прикладных исследований, приветствуются материалы, охватывающие как существующие, так и новые области биологии. С этой целью журнал опирается на эмпирические дисциплины, такие, как структурная биология, энзимология, биохимия и биофизика, а также на технологические достижения, которые позволили проводить измерения метаболомики и протеомики в массово параллельной пропускной способности и разрабатывать надежные и инновационные стратегии вычислительной биологии. Издание также признает влияние медицины и технологий, приветствует исследования в области молекулярной генетики, молекулярной диагностики и терапии, а также нанотехнологий. Цель состоит во всесторонней иллюстрации молекулярных механизмов, регулирующих белки, нуклеиновые кислоты, углеводы, липиды и мелкие метаболиты в организмах всех ветвей жизни. В дополнение к интересным новым открытиям, методам и приложениям, Frontiers in Molecular Biosciences рассмотрит также новые проверяемые гипотезы для появления различных точек зрения и стимуляции научного диалога. Интеграция подходов in silico, in vitro и in vivo в будущем может принести пользу усилиям во всех областях наук о жизни.
Пример статьи, название - CRISPR-Cas13-Mediated Knockdown of lncRNA-GACAT3 Inhibited Cell Proliferation and Motility, and Induced Apoptosis by Increasing p21, Bax, and E-Cadherin Expression in Bladder Cancer. Заголовок (Abstract) - The current study is to investigate the expression pattern and biological function of long non-coding RNA Focally gastric cancer-associated transcript3 (GACAT3) in bladder cancer. Real-time quantitative qPCR was used to detect the expression level of GACAT-3 in tumor tissues and paired normal tissues. Human bladder cancer T24 and 5637 cell lines were transiently transfected with specific CRISPR-Cas13 or negative control CRISPR-Cas13. Cell migration, proliferation, and apoptosis were measured by using wound healing assay CCK-8 assay and Caspase-3 ELISA assay, respectively. The expression changes of p21, Bax, and E-cadherin after knockdown of GACAT3 were detected by using Western blot. The results demonstrated that GACAT3 was up-regulated in bladder cancer tissues than that in the paired normal tissues. Inhibition of cell proliferation, increased apoptosis, and decreased motility were observed in T24 and 5637 cell lines transfected by CRISPR-Cas13 targeting GACAT3. Downregulation of GACAT3 increased p21, Bax, and E-cadherin expression and silencing these genes could eliminate the phenotypic changes induced by knockdown of GACAT3. A ceRNA mechanism for GACAT3 was also revealed. By using CRISPR-Cas13 biotechnology, we suggested that GACAT3 may be a novel target for diagnosis and treatment of bladder cancer.
Introduction
Bladder cancer (BC) is the most common type in malignancy tumors of the urinary system all over the world. The cause of bladder cancer is complex, which include both genetic factors and external environmental factors (Czerniak et al., 2016). Under the action of internal and external factors, the signal networks changed in the bladder epithelial cells lead to the occurrence of bladder cancer. Therefore, the development of bladder cancer is the result of a sophisticated multi-molecule effect (Sathe and Nawroth, 2018). These disrupted molecular networks are the root of the appearance of the malignant phenotypes of bladder cancer. For a long time, we have been trying to find the signal molecules which are located in the center of the signal network and attempt to achieve the goal of interfering with the progression of bladder cancer by acting on these molecules. Although traditional treatment such as surgery, chemotherapy and radiation can treat with bladder cancer to a certain extent, they usually cause severe side effect (Amit and Hochberg, 2010). Thus, it is necessary to develop a new method to deal with bladder cancer specifically.
A growing number body of evidences demonstrated that long non-coding RNAs (lncRNAs) play an important role in the pathological and physiological processes of cells, including the formation of cancers (Huarte, 2015). Compared with other types of RNA such as siRNA, piRNA, or miRNA, the mechanisms of lncRNAs are more sophisticated. Through interaction with RNAs, DNA, or other protein molecules, lncRNAs regulate the expression of many proteins (Jariwala and Sarkar, 2016). LncRNA-DILC inhibits the expression of IL-6 by binding to the IL-6 promoter DNA in hepatocellular carcinoma, thereby inhibiting the growth of cancer stem cells (Wang et al., 2016). In breast cancer, lncRNA-LINP1 was found to serve as an important regulator which enhances DNA-repair activity by interacting with DNA-PKcs and Ku80 proteins (Zhang et al., 2016). Moreover, the dysregulation of hundreds of lncRNAs are closely related to the clinical pathologies of gastric cancer in one previous research (Zhao et al., 2015).
LncRNA-GACAT3 is located on human Chr 2p24.3 and it was reported to be upregulated in some types of cancer tissues, such as gastric cancer (Feng et al., 2018), colorectal cancer (Zhou et al., 2018) and non-small cell lung cancer (Yang et al., 2018). The potential of lncRNA-GACAT3 as an important regulatory point in cancer is gradually developed. Although the role of lncRNA-GACAT3 in regulating cell function has been reported in previous studies, its biological function and molecular mechanism in BC is not clear yet (Shen et al., 2016; Feng et al., 2018; Zhou et al., 2018).
In this study, we found that lncRNA-GACAT3 was upregulated in bladder cancer and can promote malignant phenotypes for the first time. Moreover, we also found that GACAT3 can inhibit cell apoptosis, and promote cell proliferation and migration by downregulating the expression of P21, Bax, and E-cadherin proteins in bladder cancer. These results might provide a novel potential methods for targeted therapy or diagnosis of bladder cancer.
Keywords: long non-coding RNA, GACAT3, bladder cancer, CRISPR-Cas13, cancer development