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      Gossypol Induces Apoptosis of Human Pancreatic Cancer Cells via CHOP/Endoplasmic Reticulum Stress Signaling Pathway

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          Abstract

          Gossypol, a natural phenolic aldehyde present in cotton plants, was originally used as a means of contraception, but is currently being studied for its anti-proliferative and anti-metastatic effects on various cancers. However, the intracellular mechanism of action regarding the effects of gossypol on pancreatic cancer cells remains unclear. Here, we investigated the anti-cancer effects of gossypol on human pancreatic cancer cells (BxPC-3 and MIA PaCa-2). Cell counting kit-8 assays, annexin V/propidium iodide staining assays, and transmission electron microscopy showed that gossypol induced apoptotic cell death and apoptotic body formation in both cell lines. RNA sequencing analysis also showed that gossypol increased the mRNA levels of CCAAT/enhancer-binding protein homologous protein (CHOP) and activating transcription factor 3 (ATF3) in pancreatic cancer cell lines. In addition, gossypol facilitated the cleavage of caspase-3 via protein kinase RNA-like ER kinase (PERK), CHOP, and Bax/Bcl-2 upregulation in both cells, whereas the upregulation of ATF was limited to BxPC-3 cells. Finally, a three-dimensional culture experiment confirmed the successful suppression of cancer cell spheroids via gossypol treatment. Taken together, our data suggest that gossypol may trigger apoptosis in pancreatic cancer cells via the PERK-CHOP signaling pathway. These findings propose a promising therapeutic approach to pancreatic cancer treatment using gossypol.

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          TopHat: discovering splice junctions with RNA-Seq

          Cole Trapnell, Lior Pachter, Steven Salzberg (2011)
          Motivation: A new protocol for sequencing the messenger RNA in a cell, known as RNA-Seq, generates millions of short sequence fragments in a single run. These fragments, or ‘reads’, can be used to measure levels of gene expression and to identify novel splice variants of genes. However, current software for aligning RNA-Seq data to a genome relies on known splice junctions and cannot identify novel ones. TopHat is an efficient read-mapping algorithm designed to align reads from an RNA-Seq experiment to a reference genome without relying on known splice sites. Results: We mapped the RNA-Seq reads from a recent mammalian RNA-Seq experiment and recovered more than 72% of the splice junctions reported by the annotation-based software from that study, along with nearly 20 000 previously unreported junctions. The TopHat pipeline is much faster than previous systems, mapping nearly 2.2 million reads per CPU hour, which is sufficient to process an entire RNA-Seq experiment in less than a day on a standard desktop computer. We describe several challenges unique to ab initio splice site discovery from RNA-Seq reads that will require further algorithm development. Availability: TopHat is free, open-source software available from http://tophat.cbcb.umd.edu Contact: cole@cs.umd.edu Supplementary information: Supplementary data are available at Bioinformatics online.
          Article 0 comments Cited 1540 times – based on 0 reviews     Review now
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            The unfolded protein response: from stress pathway to homeostatic regulation.

            Peter Walter, David Ron (2011)
            The vast majority of proteins that a cell secretes or displays on its surface first enter the endoplasmic reticulum (ER), where they fold and assemble. Only properly assembled proteins advance from the ER to the cell surface. To ascertain fidelity in protein folding, cells regulate the protein-folding capacity in the ER according to need. The ER responds to the burden of unfolded proteins in its lumen (ER stress) by activating intracellular signal transduction pathways, collectively termed the unfolded protein response (UPR). Together, at least three mechanistically distinct branches of the UPR regulate the expression of numerous genes that maintain homeostasis in the ER or induce apoptosis if ER stress remains unmitigated. Recent advances shed light on mechanistic complexities and on the role of the UPR in numerous diseases.
            Article 0 comments Cited 1038 times – based on 0 reviews     Review now
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              Is Open Access

              Epidemiology of Pancreatic Cancer: Global Trends, Etiology and Risk Factors

              Prashanth Rawla, Tagore Sunkara, Vinaya Gaduputi (2019)
              Pancreatic cancer is the seventh leading cause of cancer-related deaths worldwide. However, its toll is higher in more developed countries. Reasons for vast differences in mortality rates of pancreatic cancer are not completely clear yet, but it may be due to lack of appropriate diagnosis, treatment and cataloging of cancer cases. Because patients seldom exhibit symptoms until an advanced stage of the disease, pancreatic cancer remains one of the most lethal malignant neoplasms that caused 432,242 new deaths in 2018 (GLOBOCAN 2018 estimates). Globally, 458,918 new cases of pancreatic cancer have been reported in 2018, and 355,317 new cases are estimated to occur until 2040. Despite advancements in the detection and management of pancreatic cancer, the 5-year survival rate still stands at 9% only. To date, the causes of pancreatic carcinoma are still insufficiently known, although certain risk factors have been identified, such as tobacco smoking, diabetes mellitus, obesity, dietary factors, alcohol abuse, age, ethnicity, family history and genetic factors, Helicobacter pylori infection, non-O blood group and chronic pancreatitis. In general population, screening of large groups is not considered useful to detect the disease at its early stage, although newer techniques and the screening of tightly targeted groups (especially of those with family history), are being evaluated. Primary prevention is considered of utmost importance. Up-to-date statistics on pancreatic cancer occurrence and outcome along with a better understanding of the etiology and identifying the causative risk factors are essential for the primary prevention of this disease.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Microbiol Biotechnol
                Journal ID (iso-abbrev): J Microbiol Biotechnol
                Title: Journal of Microbiology and Biotechnology
                Publisher: The Korean Society for Microbiology and Biotechnology
                ISSN (Print): 1017-7825
                ISSN (Electronic): 1738-8872
                Publication date (Print): 28 May 2022
                Publication date (Electronic): 23 February 2022
                Publication date PMC-release: 23 February 2022
                Volume: 32
                Issue: 5
                Pages: 645-656
                Affiliations
                [1 ]Division of Analytical Science, Korea Basic Science Institute, Daejeon 34133, Republic of Korea
                [2 ]Department of Life Science and Research Institute for Natural Sciences, College of Natural Sciences, Hanyang University, Seoul 04763, Republic of Korea
                [3 ]Microbial Research Department, Nakdonggang National Institute of Biological Resources, Sangju 37242, Republic of Korea
                [4 ]Department of Biological Engineering, Inha University, Incheon 22212, Republic of Korea
                [5 ]Department of Biotechnology, CHA University, Seongnam 13488, Republic of Korea
                [6 ]Laboratory of Chemical Biology and Genomics, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Republic of Korea
                Author notes
                [* ] Corresponding author Phone: +82-42-860-4563 E-mail: hjjang0228@ 123456gmail.com
                Article
                Publisher ID: jmb-32-5-645
                DOI: 10.4014/jmb.2110.10019
                PMC ID: 9628887
                PubMed ID: 35283426
                SO-VID: 73773eeb-dcb5-45be-9e16-98e718ffbccd
                Copyright © Copyright © 2022 by the authors. Licensee KMB.
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license.

                History
                Date received : 13 October 2021
                Date revision received : 4 February 2022
                Date accepted : 21 February 2022
                Categories
                Subject: Research article
                Subject: Biotechnology and Bioengineering (BB)
                Subject: Bioactive Compounds and Functional Foods

                Keywords: gossypol,pancreatic cancer,apoptosis,ccaat/enhancer-binding protein homologous protein,endoplasmic reticulum stress
                Data availability:
                Keywords: gossypol, pancreatic cancer, apoptosis, ccaat/enhancer-binding protein homologous protein, endoplasmic reticulum stress

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