BMC Molecular and Cell Biology最新文献

{"title":"Effect of Emi1 gene silencing on the proliferation and invasion of human breast cancer cells.","authors":"Ying Kuang, Shengwen Huang, Shifan Tang, Zhaozhen Zhuo, Keyan Linghu","doi":"10.1186/s12860-023-00494-1","DOIUrl":"10.1186/s12860-023-00494-1","url":null,"abstract":"<p><p>Breast cancer is the most common malignant tumour in women. The early silk-splitting inhibitor protein 1 Emi1 is responsible for mediating ubiquitin protein degradation. The present study investigated the effects of the decreased expression of the Emil gene on the proliferation and invasion of breast cancer cells. The interference efficiency of small interfering ribonucleic acid (siRNA) was quantitatively verified using fluorescence real-time quantitative polymerase chain reaction (RT-qPCR) and Western blotting, and the effect of Emi1 gene silencing on cell vitality and invasion was determined using MTT and Transwell assays, respectively. The expression of the proliferation genes programmed cell death receptor 4 (PDCD-4), fatty acid synthase ligand (FasL), PTEN and RhoB, along with the invasive genes Maspin, TIMP3 and RECK, was measured using fluorescence RT-qPCR. In breast cancer cells, siRNA successfully reduced the expression of the Emi1 gene, and the expression level of the cell proliferation genes PDCD-4, FasL, PTEN and RhoB, along with invasive genes Maspin, TIMP3 and RECK, decreased significantly (P < 0.05). Furthermore, Emi1 gene silencing reduced the proliferation and invasion abilities of MDA-MB-231 and SUM149PT cells by reducing the expression of proliferative and invasive genes.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"24 1","pages":"34"},"PeriodicalIF":2.8,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10690968/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138469895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TNFα induces Caspase-3 activity in hematopoietic progenitor cells CD34+, CD33+, and CD41 + of myelodysplastic syndromes.","authors":"Anggraini Iriani, Andhika Rachman, Rahayuningsih D Setiabudy, Siti B Kresno, Aru W Sudoyo, Mansyur Arief, Alida R Harahap, Marsya Kaila Fatina","doi":"10.1186/s12860-023-00495-0","DOIUrl":"10.1186/s12860-023-00495-0","url":null,"abstract":"<p><strong>Background: </strong>Cytopenia is the primary feature of Myelodysplastic Syndrome, even in the presence of hypercellular bone marrow. TNFα is recognized as both a proinflammatory, and proapoptotic cytokine with a well established role in promoting apoptosis in MDS. Therefore, TNFα has the potential to be a valuable biomarker for predicting the progression of cytopenia in MDS. This study aims to establish the role of TNFα exposure in triggering apoptosis through caspase-3 activity in CD34+, CD33+, and CD41 + cells in MDS.</p><p><strong>Methods: </strong>This study is an in vitro comparative experimental research. Bone marrow mononuclear cells were isolated as the source of hematopoietic progenitor cells. Subsequently, CD34+, CD33+, and CD41 + cells were exposed to rhTNFα, and the caspase-3 activity was measured using flowcytometry.</p><p><strong>Results: </strong>In MDS CD33 + and CD41 + caspase-3 activity of rhTNFα exposed cells was significantly higher than without exposed cells. The opposite result was found in CD34 + cells, where the caspase-3 activity without rhTNFα exposed cells was significantly higher than rhTNFα exposed cells.</p><p><strong>Conclusion: </strong>rhTNFα exposure led to an elevation in caspase-3 activity in MDS progenitor cells, especially in those that had differentiated into myeloid cell CD33 + and megakaryocyte cell CD41+, as opposed to the early progenitor cells CD34+.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"24 1","pages":"33"},"PeriodicalIF":2.8,"publicationDate":"2023-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10662645/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138290314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From network analysis to experimental validation: identification of regulators of non-muscle myosin II contractility using the folded-gastrulation signaling pathway.","authors":"Andy Zhao, Sophia Varady, Madelyn O'Kelley-Bangsberg, Vicki Deng, Amy Platenkamp, Petra Wijngaard, Miriam Bern, Wyatt Gormley, Elaine Kushkowski, Kat Thompson, Logan Tibbetts, A Tamar Conner, David Noeckel, Aidan Teran, Anna Ritz, Derek A Applewhite","doi":"10.1186/s12860-023-00492-3","DOIUrl":"10.1186/s12860-023-00492-3","url":null,"abstract":"<p><p>The morphogenetic process of apical constriction, which relies on non-muscle myosin II (NMII) generated constriction of apical domains of epithelial cells, is key to the development of complex cellular patterns. Apical constriction occurs in almost all multicellular organisms, but one of the most well-characterized systems is the Folded-gastrulation (Fog)-induced apical constriction that occurs in Drosophila. The binding of Fog to its cognizant receptors Mist/Smog results in a signaling cascade that leads to the activation of NMII-generated contractility. Despite our knowledge of key molecular players involved in Fog signaling, we sought to explore whether other proteins have an undiscovered role in its regulation. We developed a computational method to predict unidentified candidate NMII regulators using a network of pairwise protein-protein interactions called an interactome. We first constructed a Drosophila interactome of over 500,000 protein-protein interactions from several databases that curate high-throughput experiments. Next, we implemented several graph-based algorithms that predicted 14 proteins potentially involved in Fog signaling. To test these candidates, we used RNAi depletion in combination with a cellular contractility assay in Drosophila S2R + cells, which respond to Fog by contracting in a stereotypical manner. Of the candidates we screened using this assay, two proteins, the serine/threonine phosphatase Flapwing and the putative guanylate kinase CG11811 were demonstrated to inhibit cellular contractility when depleted, suggestive of their roles as novel regulators of the Fog pathway.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"24 1","pages":"32"},"PeriodicalIF":2.8,"publicationDate":"2023-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10568788/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41191061","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Simple, low-cost, and well-performing method, the outgrowth technique, for the isolation of cells from nasal polyps.","authors":"Jonghui Kim, Karla Hegener, Claudia Hagedorn, Daniel Weidinger, Kashin Jamal Jameel, Inga Marte Charlott Seuthe, Sabine Eichhorn, Florian Kreppel, Jonas Jae-Hyun Park, Jürgen Knobloch","doi":"10.1186/s12860-023-00493-2","DOIUrl":"10.1186/s12860-023-00493-2","url":null,"abstract":"<p><strong>Background: </strong>Epithelial cells are an important part of the pathomechanism in chronic rhinosinusitis with nasal polyps. It is therefore essential to establish a robust method for the isolation and culture of epithelial cells from nasal polyps to enable further research. In this study, the feasibility of the outgrowth technique for the isolation of the epithelial cells from the nasal polyps was evaluated.</p><p><strong>Results: </strong>Using the outgrowth technique, epithelial cells could be isolated from all tissue samples. Isolated epithelial cells showed a proliferation rate of approximately 7- to 23-fold every 6 days up to the 3rd passage. Over 97% of isolated cells were shown to be cytokeratin- and p63-positive, and over 86% of them were Ki-67-positive in flow cytometry. Interleukin-33 and periostin were detectable in the supernatant.</p><p><strong>Conclusions: </strong>We introduce a simple, low-cost, and well-performing method for isolating epithelial cells from nasal polyps with the outgrowth technique.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"24 1","pages":"31"},"PeriodicalIF":2.8,"publicationDate":"2023-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10566096/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41191062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive brain tissue metabolomics and biological network technology to decipher the mechanism of hydrogen-rich water on Radiation-induced cognitive impairment in rats.","authors":"Xiaoming Liu, Mengya Liu, Huan Liu, Hui Yuan, Yong Wang, Xiaoman Chen, Jianguo Li, Xiujun Qin","doi":"10.1186/s12860-023-00491-4","DOIUrl":"10.1186/s12860-023-00491-4","url":null,"abstract":"<p><strong>Background: </strong>Hydrogen-rich water (HRW) has been shown to prevent cognitive impairment caused by ionizing radiation. This study aimed to investigate the pharmacological effects and mechanisms of HRW on ionizing radiation by coupling the brain metabolomics and biological target network methods.</p><p><strong>Methods and results: </strong>HRW significantly improves the cognitive impairment in rats exposed to ionizing radiation. Based on metabolomics and biological network results, we identified 54 differential metabolites and 93 target genes. The KEGG pathway indicates that glutathione metabolism, ascorbic acid and aldehyde acid metabolism, pentose and glucuronic acid interconversion, and glycerophospholipid metabolism play important roles in ionizing radiation therapy.</p><p><strong>Conclusion: </strong>Our study has systematically elucidated the molecular mechanism of HRW against ionizing radiation, which can be mediated by modulating targets, pathways and metabolite levels. This provides a new perspective for identifying the underlying pharmacological mechanism of HRW.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"24 1","pages":"30"},"PeriodicalIF":2.8,"publicationDate":"2023-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10523633/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41105908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mineral elements and adiposity-related consequences in adolescents with intellectual disabilities.","authors":"Ahmad H Alghadir, Sami A Gabr, Amir Iqbal","doi":"10.1186/s12860-023-00490-5","DOIUrl":"10.1186/s12860-023-00490-5","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Patients with intellectual disabilities are shown to have a limited capacity for cooperation, communication,and other biological consequences, which significantly require a specialized interest in healthcare professionals worldwide.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Aim: &lt;/strong&gt;In this respect, the present study was designed to evaluate the levels mineral elements, and their correlation with oxidative stress markers and adiposity markers; leptin (L), adiponectin (A), and L/A ratio in adolescents with intellectual disabilities.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;A total of 350 schoolchildren aged (12-18 years) were randomly invited to participate in this prospective, observational study. Only 300 participants agreed to participate in this study. According to Intelligence quotients scores (IQ) measured by WISC-III, the participants were classified into two groups; the healthy control group (no = 180; IQ = 90-114); and the moderate intellectual disability (MID) group (no = 120; IQ = 35-49). Adiposity markers; body mass index (BMI), waist-to-hip ratio (WHR), waist-to-height ratio (WHtR), physical activity scores, adipokines biomarkers; leptin, adiponectin, L/A ratio, oxidative stress, and plasma mineral elements were evaluated by prevalidated questionnaires, inductively coupled plasma-mass spectrometry (ICP-MS), colorimetric, and immunoassay techniques.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Intellectual disability of moderate type was reported in 40% of the studied populations most of them are men aged 12-18 years (66.6% for men vs. 33.3 for females). Obesity was shown to be associated with the degree of intellectual disability of the students. There was a significant (P = 0.001) increase in the BMI, WHR, and WHtR scores as obesity markers with poor physical activity (P = 0.01) in students with poor disability compared to healthy controls (HC). The levels of leptin (P = 0.001), adiponectin (P = 0.01), and L/A ratio (P = 0.01) as adiposity biomarkers were significantly increased in students with MID compared to healthy controls. Also, oxidative stress measured by malondialdehyde (MDA) (P = 0.01) and total antioxidant capacity (TAC) (P = 0.01) were significantly increased in students with MID compared to healthy control subjects. In addition, mineral elements were shown to be linked with intellectual disability. The data showed that the levels of Fe, Mn, Zn, Hg, Pb, Ca, Cr, Mg, and Ni significantly (P = 0.001) increased, and the levels of Al, Na, K, Cu, and Zn/Cu ratio significantly (P = 0.001) decreased in subjects with MID compared to healthy controls. Correlation analysis concluded that changes in mineral elements significantly correlated with adiposity markers, oxidative stress, and the scores of intellectual disability (WISC III-IQ score).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;The intellectual disability of moderate type (MID) was associated with abnormal changes in the levels of essential mineral elements and adipokines and increased levels of ","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"24 1","pages":"29"},"PeriodicalIF":2.8,"publicationDate":"2023-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10512604/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41123963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glycyrrhizin inhibits LPS-induced inflammatory responses in goat ruminal epithelial cells in vitro.","authors":"Junfeng Liu, Bei Ma, Guang Hao, DuoDuo Su, Tianyang Wang, Ze Ding, Xuefeng Guo","doi":"10.1186/s12860-023-00489-y","DOIUrl":"10.1186/s12860-023-00489-y","url":null,"abstract":"<p><p>Inflammation plays a crucial role in the progression of Subacute Ruminal Acidosis (SARA). The experiment was designed to investigate anti-inflammatory effects of glycyrrhizin on goats ruminal epithelial cells (GREC) which were induced SARA by Lipopolysaccharide (LPS) in vitro. The GREC were induced SARA by adding LPS at the concentration of 5 μm and glycyrrhizin was added at different concentration of 0, 60, 90, 120, 150 μm. The structural integrity of LPS-induced GREC with the treatment of glycyrrhizin were observed by electron microscope; The levels of inflammatory factors TNF-α, IL-1β, IL-6, IL-8 and IL-12 were measured by ELISA; The number of Zo-1 and Occludin were measured, the expression of tight junction protein Occludin were measured by Western blot, and the mRNA expression of NF-κB, TNF-α, IL-1β, IL-6, IL-8 and IL-12 were measured in vitro. The results showed that higher concentration treatment of glycyrrhizin led to better morphology in LPS-induced GREC. Glycyrrhizin inhibited the growth of inflammatory factors TNF-α, IL-1β, IL-6, IL-8 and IL-12 in a dose-dependent manner. The number of ZO-1 and Occludin increased with the increase of adding of glycyrrhizin. Western blot analysis showed that the expression of tight junction protein Occludin in LPS-induced GREC increased with the adding of glycyrrhizin in a dose-dependent manner. Furthermore, the mRNA expression of NF-κB, TNF-α, IL-1β, IL-6, IL-8 and IL-12 decreased significantly with the increase treatment of glycyrrhizin. Glycyrrhizin significantly inhibits LPS-induced inflammatory mediators in GREC and the effects are better with the increase treatment of glycyrrhizin in vitro.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"24 1","pages":"28"},"PeriodicalIF":2.8,"publicationDate":"2023-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10507872/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41111126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"D-galactose-induced mitochondrial oxidative damage and apoptosis in the cochlear stria vascularis of mice.","authors":"Zhe Peng, Chunli Zhao, Zijing Yang, Shusheng Gong, Zhengde Du","doi":"10.1186/s12860-023-00480-7","DOIUrl":"10.1186/s12860-023-00480-7","url":null,"abstract":"<p><strong>Background: </strong>Age-related hearing loss, known as presbycusis, is the result of auditory system degeneration. Numerous studies have suggested that reactive oxygen species (ROS) and mitochondrial oxidative damage play important roles in the occurrence and progression of aging. The D-galactose (D-gal)-induced aging model is well known and widely utilized in aging research. Our previous studies demonstrate that administration of D-gal causes mitochondrial oxidative damage and causes subsequent dysfunction in the cochlear ribbon synapses, which in turn leads to hearing changes and early stage presbycusis. Stria vascularis (SV) cells are vital for hearing function. However, it is unclear to what extent D-gal induces oxidative damage and apoptosis in the cochlear SV of mice. In addition, the source of the causative ROS in the cochlear SV has not been fully investigated.</p><p><strong>Methods: </strong>In this study, we investigated ROS generation in the cochlear SV of mice treated with D-gal. Hearing function was measured using the auditory brainstem response (ABR). Immunofluorescence was used to examine apoptosis and oxidative damage. Transmission electron microscopy was also used to investigate the mitochondrial ultrastructure. DNA fragmentation was determined using the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) assay. Mitochondrial membrane potential (MMP) and ATP were also measured.</p><p><strong>Results: </strong>We found that D-gal-treated mice exhibited a significant shift in the mean amplitude and latency of the ABR; a remarkable increase in the levels of NADPH oxidase (NOX-2), Uncoupling protein 2 (UCP2) and cleaved caspase-3 (c-Cas3) was observed, as well as an increase in the number of TUNEL-positive cells were observed in the SV of mice. Both the expression of the DNA oxidative damage biomarker 8-hydroxy-2-deoxyguanosine (8-OHdG) and a commonly occurring mitochondrial DNA deletion were markedly elevated in the SV of mice that had been treated with D-gal to induce aging. Conversely, the ATP level and MMP were significantly reduced in D-gal-induced aging mice. We also found alterations in the mitochondrial ultrastructure in the SV of aging mice, which include swollen and distorted mitochondrial shape, shortened and thickened microvilli, and the accumulation of lysosomes in the SV.</p><p><strong>Conclusion: </strong>Our findings suggest that the impairment of cochlear SV during presbycusis may be caused by mitochondrial oxidative damage and subsequent apoptosis.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"24 1","pages":"27"},"PeriodicalIF":2.8,"publicationDate":"2023-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10441755/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10056175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Keratin 19 binds and regulates cytoplasmic HNRNPK mRNA targets in triple-negative breast cancer.","authors":"Arwa Fallatah, Dimitrios G Anastasakis, Amirhossein Manzourolajdad, Pooja Sharma, Xiantao Wang, Alexis Jacob, Sarah Alsharif, Ahmed Elgerbi, Pierre A Coulombe, Markus Hafner, Byung Min Chung","doi":"10.1186/s12860-023-00488-z","DOIUrl":"10.1186/s12860-023-00488-z","url":null,"abstract":"<p><strong>Background: </strong>Heterogeneous nuclear ribonucleoprotein K (HNRNPK) regulates pre-mRNA processing and long non-coding RNA localization in the nucleus. It was previously shown that shuttling of HNRNPK to the cytoplasm promotes cell proliferation and cancer metastasis. However, the mechanism of HNRNPK cytoplasmic localization, its cytoplasmic RNA ligands, and impact on post-transcriptional gene regulation remain uncharacterized.</p><p><strong>Results: </strong>Here we show that the intermediate filament protein Keratin 19 (K19) directly interacts with HNRNPK and sequesters it in the cytoplasm. Correspondingly, in K19 knockout breast cancer cells, HNRNPK does not localize in the cytoplasm, resulting in reduced cell proliferation. We comprehensively mapped HNRNPK binding sites on mRNAs and showed that, in the cytoplasm, K19-mediated HNRNPK-retention increases the abundance of target mRNAs bound to the 3' untranslated region (3'UTR) at the expected cytidine-rich (C-rich) sequence elements. Furthermore, these mRNAs protected by HNRNPK in the cytoplasm are typically involved in cancer progression and include the p53 signaling pathway that is dysregulated upon HNRNPK knockdown (HNRNPK KD) or K19 knockout (KRT19 KO).</p><p><strong>Conclusions: </strong>This study identifies how a cytoskeletal protein can directly regulate gene expression by controlling the subcellular localization of RNA-binding proteins to support pathways involved in cancer progression.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"24 1","pages":"26"},"PeriodicalIF":2.8,"publicationDate":"2023-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10433649/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10421813","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A computational peptide model induces cancer cells' apoptosis by docking Kringle 5 to GRP78.","authors":"Ibrahim Khater, Aaya Nassar","doi":"10.1186/s12860-023-00484-3","DOIUrl":"10.1186/s12860-023-00484-3","url":null,"abstract":"<p><strong>Background: </strong>Cells can die through a process called apoptosis in both pathological and healthy conditions. Cancer development and progression may result from abnormal apoptosis. The 78-kDa glucose-regulated protein (GRP78) is increased on the surface of cancer cells. Kringle 5, a cell apoptosis agent, is bound to GRP78 to induce cancer cell apoptosis. Kringle 5 was docked to GRP78 using ClusPro 2.0. The interaction between Kringle 5 and GRP78 was investigated.</p><p><strong>Results: </strong>The interacting amino acids were found to be localized in three areas of Kringle 5. The proposed peptide is made up of secondary structure amino acids that contain Kringle 5 interaction residues. The 3D structure of the peptide model amino acids was created using the PEP-FOLD3 web tool.</p><p><strong>Conclusions: </strong>The proposed peptide completely binds to the GRP78 binding site on the Kringle 5, signaling that it might be effective in the apoptosis of cancer cells.</p>","PeriodicalId":9099,"journal":{"name":"BMC Molecular and Cell Biology","volume":"24 1","pages":"25"},"PeriodicalIF":2.8,"publicationDate":"2023-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10408047/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10019395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}