Journal of cellular biochemistry最新文献

{"title":"Perilipins: A family of five fat-droplet storing proteins that play a significant role in fat homeostasis","authors":"Preethi Chandrasekaran,&nbsp;Sabine Weiskirchen,&nbsp;Ralf Weiskirchen","doi":"10.1002/jcb.30579","DOIUrl":"10.1002/jcb.30579","url":null,"abstract":"<p>Lipid droplets are organelles with unique spherical structures. They consist of a hydrophobic neutral lipid core that varies depending on the cell type and tissue. These droplets are surrounded by phospholipid monolayers, along with heterogeneous proteins responsible for neutral lipid synthesis and metabolism. Additionally, there are specialized lipid droplet-associated surface proteins. Recent evidence suggests that proteins from the perilipin family (PLIN) are associated with the surface of lipid droplets and are involved in their formation. These proteins have specific roles in hepatic lipid droplet metabolism, such as protecting the lipid droplets from lipase action and maintaining a balance between lipid storage and utilization in specific cells. Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterized by the accumulation of lipid droplets in more than 5% of the hepatocytes. This accumulation can progress into metabolic dysfunction-associated steatohepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma. The accumulation of hepatic lipid droplets in the liver is associated with the progression of MASLD and other diseases such as sarcopenic obesity. Therefore, it is crucial to understand the role of perilipins in this accumulation, as these proteins are key targets for developing novel therapeutic strategies. This comprehensive review aims to summarize the structure and characteristics of PLIN proteins, as well as their pathogenic role in the development of hepatic steatosis and fatty liver diseases.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 6","pages":""},"PeriodicalIF":4.0,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30579","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140922327","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":"PCSK9 inhibitors as safer therapeutics for atherosclerotic cardiovascular disease (ASCVD): Pharmacophore design and molecular dynamics analysis","authors":"Ibrahim O. Kehinde,&nbsp;Oluwole Akawa,&nbsp;Adeniyi T. Adewumi,&nbsp;Ali H. Rabbad,&nbsp;Mahmoud E. S. Soliman","doi":"10.1002/jcb.30581","DOIUrl":"10.1002/jcb.30581","url":null,"abstract":"<p>Cardiovascular disorders are still challenging and are among the deadly diseases. As a major risk factor for atherosclerotic cardiovascular disease, dyslipidemia, and high low-density lipoprotein cholesterol in particular, can be prevented primary and secondary by lipid-lowering medications. Therefore, insights are still needed into designing new drugs with minimal side effects. Proprotein convertase subtilisin/kexin 9 (PCSK9) enzyme catalyses protein-protein interactions with low-density lipoprotein, making it a critical target for designing promising inhibitors compared to statins. Therefore, we screened for potential compounds using a redesigned PCSK9 conformational behaviour to search for a significantly extensive chemical library and investigated the inhibitory mechanisms of the final compounds using integrated computational methods, from ligand essential functional group screening to all-atoms MD simulations and MMGBSA-based binding free energy. The inhibitory mechanisms of the screened compounds compared with the standard inhibitor. K31 and K34 molecules showed stronger interactions for PCSK9, having binding energy (kcal/mol) of −33.39 and −63.51, respectively, against −27.97 of control. The final molecules showed suitable drug-likeness, non-mutagenesis, permeability, and high solubility values. The C-α atoms root mean square deviation and root mean square fluctuation of the bound-PCSK9 complexes showed stable and lower fluctuations compared to apo PCSK9. The findings present a model that unravels the mechanism by which the final molecules proposedly inhibit the PCSK9 function and could further improve the design of novel drugs against cardiovascular diseases.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 7","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30581","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140922305","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":"Molecular insights into the antioxidant and anticancer properties: A comprehensive analysis through molecular modeling, docking, and dynamics studies","authors":"Hamza Serina Banu,&nbsp;Ismail sheriff Parvin,&nbsp;Subramanian Deepika Priyadharshini,&nbsp;Ekambaram Gayathiri,&nbsp;Palanisamy Prakash,&nbsp;Thangaraj Pratheep","doi":"10.1002/jcb.30564","DOIUrl":"10.1002/jcb.30564","url":null,"abstract":"<p>Plants are rich sources of therapeutic compounds that often lack the side effects commonly found in synthetic chemicals. Researchers have effectively synthesized pharmaceuticals from natural sources, taking inspiration from traditional medicine, in their pursuit of modern drugs. This study aims to evaluate the phenolic and flavonoid content of <i>Solanum virginianum</i> seeds using different solvent extracts, enzymatic assays including 2,2-diphenyl-1-picrylhydrazyl activity, reducing power, and superoxide activity. Our phytochemical screening identified active compounds, such as phenols, flavonoids, tannins, and alkaloids. The methanol extract notably possesses higher levels of total phenolic and flavonoid content in comparison to the other extracts. The results highlight the superior antioxidant activity of methanol-extracted leaves, demonstrated by their exceptional IC₅₀ values, which surpass the established standard. In this study, molecular docking techniques were used to assess the binding affinity and to predict the binding conformation of the compounds. Quercetin 3-O beta-<span>d</span>-galactopyranoside displayed a binding energy of −8.35 kcal/mol with several important amino acid residues, PHE222, TRP440, ILE184, LEU192, VAL221, LEU218, SER185, and ALA188. Kaempferol 3-O-beta-<span>l</span>-glucopyranoside exhibited a binding energy of −8.33 kcal/mol, interacting with specific amino acid residues including ALA 441, VAL318, VAL322, MET307, ILI409, GLY442, and PHE439. The results indicate that the methanol extract has a distinct composition of biologically active constituents compared to the other extracts. Overall, seeds exhibit promise as natural antioxidants and potential agents for combating cancer. This study highlights the significance of utilizing the therapeutic capabilities of natural compounds and enhancing our comprehension of their pharmacological characteristics.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 10","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140922303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TLR4/7-mediated host-defense responses of gingival epithelial cells","authors":"Norika Chiba,&nbsp;Ryohei Tada,&nbsp;Tomokazu Ohnishi,&nbsp;Tetsuya Matsuguchi","doi":"10.1002/jcb.30576","DOIUrl":"10.1002/jcb.30576","url":null,"abstract":"<p>Gingival epithelial cells (GECs) are physical and immunological barriers against outward pathogens while coping with a plethora of non-pathogenic commensal bacteria. GECs express several members of Toll-like receptors (TLRs) and control subsequent innate immune responses. TLR4 senses lipopolysaccharide (LPS) while TLR7/8 recognizes single-strand RNA (ssRNA) playing important roles against viral infection. However, their distinct roles in GECs have not been fully demonstrated. Here, we analyzed biological responses of GECs to  LPS and CL075, a TLR7/8 agonist. GE1, a mouse gingival epithelial cell line, constitutively express TLR4 and TLR7, but not TLR8, like primary skin keratinocytes. Stimulation of GE1 cells with CL075 induced cytokine, chemokine, and antimicrobial peptide  expressions, the pattern of which is rather different from that with LPS: higher mRNA levels of interferon (IFN) β, CXCL10, and β-defensin (BD) 14 (mouse homolog of human BD3); lower levels of tumor necrosis factor (TNF), CCL5, CCL11, CCL20, CXCL2, and CX3CL1. As for the intracellular signal transduction of GE1 cells, CL075 rapidly induced significant AKT phosphorylation but failed to activate IKKα/β-NFκB pathway, whereas LPS induced marked IKKα/β-NFκB activation without significant AKT phosphorylation. In contrast, both CL075 and LPS induced rapid IKKα/β-NFκB activation and AKT phosphorylation in a macrophage cell line. Furthermore, specific inhibition of AKT activity abrogated CL075-induced IFNβ, CXCL10, and BD14 mRNA expression in GE1 cells. Thus, TLR4/7 ligands appear to induce rather different host-defense responses of GECs through distinct intracellular signaling mechanisms.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 7","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30576","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140898534","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":"Retraction","authors":"","doi":"10.1002/jcb.30548","DOIUrl":"10.1002/jcb.30548","url":null,"abstract":"<p><b>Retraction: “(2R,3R)Dihydromyricetin inhibits osteoclastogenesis and bone loss through scavenging LPS-induced oxidative stress and NF-κB and MAPKs pathways activating,”</b> by Xuejun Zhang, Xin Li, Jianguo Fang, Xiaolong Hou, Huang Fang, Fengjing Guo, Feng Li, Anmin Chen, Shilong Huang, <i>J Cell Biochem</i> 2018, 119: 8981-8995. The above article, published online on 4 August 2018 in Wiley Online Library (https://onlinelibrary.wiley.com/doi/full/10.1002/jcb.27154) has been retracted by agreement between the journal's Editor in Chief, Christian Behl, and Wiley Periodicals LLC.</p><p>The retraction has been agreed following an investigation based on allegations raised by third parties. During the investigation, several flaws and inconsistencies were found within the data presented. Thus, the editors consider the conclusions of this article to be invalid. The authors have been informed of the retraction but were not available for a final confirmation.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 9","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30548","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140891599","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":"Heterogeneous nuclear ribonucleoprotein A3 binds to the internal ribosomal entry site of enterovirus A71 and affects virus replication in neural cells","authors":"Jhao-Yin Lin,&nbsp;Jing-Yi Lin,&nbsp;Rei-Lin Kuo,&nbsp;Hsing-I Huang","doi":"10.1002/jcb.30575","DOIUrl":"10.1002/jcb.30575","url":null,"abstract":"<p>Enterovirus A71 (EV-A71) belongs to the genus <i>Enterovirus</i> of the Picornaviridae family and often causes outbreaks in Asia. EV-A71 infection usually causes hand, foot, and mouth disease and can even affect the central nervous system, causing neurological complications or death. The 5′-untranslated region (5′-UTR) of EV-A71 contains an internal ribosome entry site (IRES) that is responsible for the translation of viral proteins. IRES-transacting factors can interact with the EV-A71 5′-UTR to regulate IRES activity. Heterogeneous nuclear ribonucleoprotein (hnRNP) A3 is a member of the hnRNP A/B protein family of RNA-binding proteins and is involved in RNA transport and modification. We found that hnRNP A3 knockdown promoted the replication of EV-A71 in neural calls. Conversely, increasing the expression of hnRNP A3 within cells inhibits the growth of EV-A71. HnRNP A3 can bind to the EV-A71 5′-UTR, and knockdown of hnRNP A3 enhances the luciferase activity of the EV-A71 5′-UTR IRES. The localization of hnRNP A3 shifts from the nucleus to the cytoplasm of infected cells during viral infection. Additionally, EV-A71 infection can increase the protein expression of hnRNP A3, and the protein level is correlated with efficient viral growth. Based on these findings, we concluded that hnRNP A3 plays a negative regulatory role in EV-A71 replication within neural cells.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 12","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140891653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interplay of RUNX2 and KLF4 in initial commitment of odontoblast differentiation","authors":"Yongyan Gao,&nbsp;Yuxiu Lin,&nbsp;Yuanyuan Li,&nbsp;Wenrui Zeng,&nbsp;Zhi Chen","doi":"10.1002/jcb.30577","DOIUrl":"10.1002/jcb.30577","url":null,"abstract":"<p>Odontoblast differentiation is a key process in dentin formation. Mouse dental papilla cells (mDPCs) are pivotal in dentinogenesis through their differentiation into odontoblasts. Odontoblast differentiation is intricately controlled by transcription factors (TFs) in a spatiotemporal manner. Previous research explored the role of RUNX2 and KLF4 in odontoblast lineage commitment, respectively. Building on bioinformatics analysis of our previous ATAC-seq profiling, we hypothesized that KLF4 potentially collaborates with RUNX2 to exert its biological role. To investigate the synergistic effect of multiple TFs in odontoblastic differentiation, we first examined the spatiotemporal expression patterns of RUNX2 and KLF4 in dental papilla at the bell stage using immunostaining techniques. Notably, RUNX2 and KLF4 demonstrated colocalization in preodontoblast. Further, immunoprecipitation and proximity ligation assays verified the interaction between RUNX2 and KLF4 in vitro. Specifically, the C-terminus of RUNX2 was identified as the interacting domain with KLF4. Functional implications of this interaction were investigated using small hairpin RNA-mediated knockdown of <i>Runx2</i>, <i>Klf4</i>, or both. Western blot analysis revealed a marked decrease in DSPP expression, an odontoblast differentiation marker, particularly in the double knockdown condition. Additionally, alizarin red S staining indicated significantly reduced mineralized nodule formation in this group. Collectively, our findings highlight the synergistic interaction between RUNX2 and KLF4 in promoting odontoblast differentiation from mDPCs. This study contributes to a more comprehensive understanding of the regulatory network of TFs governing odontoblast differentiation.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 7","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140891591","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ZNF469 is a profibrotic regulator of extracellular matrix in hepatic stellate cells","authors":"Chaiyaboot Ariyachet,&nbsp;Archittapon Nokkeaw,&nbsp;Bootsakorn Boonkaew,&nbsp;Pisit Tangkijvanich","doi":"10.1002/jcb.30578","DOIUrl":"10.1002/jcb.30578","url":null,"abstract":"<p>Activation of quiescent hepatic stellate cells (HSCs) into proliferative myofibroblasts drives extracellular cellular matrix (ECM) accumulation and liver fibrosis; nevertheless, the transcriptional network that promotes such a process is not completely understood. ZNF469 is a putative C2H2 zinc finger protein that may bind to specific genome sequences. It is found to be upregulated upon HSC activation; however, the molecular function of ZNF469 is completely unknown. Here, we show that knockdown of ZNF469 in primary human HSCs impaired proliferation, migration, and collagen production. Conversely, overexpression of ZNF469 in HSCs yielded the opposite results. Transforming growth factor-β 1 promoted expression of ZNF469 in a Smad3-dependent manner, where the binding of Smad3 was confirmed at the ZNF469 promoter. RNA sequencing data of ZNF469-knockdown HSCs revealed the ECM-receptor interaction, which provides structural and signaling support to cells, was the most affected pathway, and significant downregulation of various collagen and proteoglycan genes was observed. To investigate the function of ZNF469, we cloned a full-length open reading frame of ZNF469 with an epitope tag and identified a nuclear localization of the protein. Luciferase reporter and chromatin immunoprecipitation assays revealed the presence of ZNF469 at the promoter of ECM genes, supporting its function as a transcription factor. Analysis of human fibrotic and cirrhotic tissues showed increased expression of ZNF469 and a positive correlation between expression levels of ZNF469 and ECM genes. Moreover, this observation was similar in other fibrotic organs, including the heart, lung, and skin, suggesting that myofibroblasts from various origins generally require ZNF469 to promote ECM production. Together, this study is the first to reveal the role of ZNF469 as a profibrotic factor in HSCs and suggests ZNF469 as a novel target for antifibrotic therapy.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 7","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140859206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Paraoxonase-2 shRNA-mediated gene silencing suppresses proliferation and migration, while promotes chemosensitivity in clear cell renal cell carcinoma cell lines","authors":"Valentina Schiavoni,&nbsp;Monica Emanuelli,&nbsp;Roberto Campagna,&nbsp;Monia Cecati,&nbsp;Davide Sartini,&nbsp;Giulio Milanese,&nbsp;Andrea Benedetto Galosi,&nbsp;Valentina Pozzi,&nbsp;Eleonora Salvolini","doi":"10.1002/jcb.30572","DOIUrl":"10.1002/jcb.30572","url":null,"abstract":"<p>Clear cell renal cell carcinoma (ccRCC) represents the most common subtype of renal tumor. Despite recent advances in identifying novel target molecules, the prognosis of patients with ccRCC continues to be poor, mainly due to the lack of sensitivity to chemo- and radiotherapy and because of one-third of renal cell carcinoma patients displays metastatic disease at diagnosis. Thus, identifying new molecules for early detection and for developing effective targeted therapies is mandatory. In this work, we focused on paraoxonase-2 (PON2), an intracellular membrane-bound enzyme ubiquitously expressed in human tissues, whose upregulation has been reported in a variety of malignancies, thus suggesting its possible role in cancer cell survival and proliferation. To investigate PON2 involvement in tumor cell metabolism, human ccRCC cell lines were transfected with plasmid vectors coding short harpin RNAs targeting PON2 transcript and the impact of PON2 silencing on cell viability, migration, and response to chemotherapeutic treatment was then explored. Our results showed that PON2 downregulation was able to trigger a decrease in proliferation and migration of ccRCC cells, as well as an enhancement of cell sensitivity to chemotherapy. Thus, taken together, data reported in this study suggest that the enzyme may represent an interesting therapeutic target for ccRCC.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 7","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140850373","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Concurrent inhibition of IR, ITGB1, and CD36 perturbated the interconnected network of energy metabolism and epithelial-to-mesenchymal transition in breast cancer cells","authors":"Thirukumaran Kandasamy,&nbsp;Shilpi Sarkar,&nbsp;Plaboni Sen,&nbsp;Dheepika Venkatesh,&nbsp;Siddhartha Sankar Ghosh","doi":"10.1002/jcb.30574","DOIUrl":"10.1002/jcb.30574","url":null,"abstract":"<p>Altered energy metabolism is an emerging hallmark of cancer and plays a pivotal in cell survival, proliferation, and biosynthesis. In a rapidly proliferating cancer, energy metabolism acts in synergism with epithelial-to-mesenchymal transition (EMT), enabling cancer stemness, dissemination, and metastasis. In this study, an interconnected functional network governing energy metabolism and EMT signaling pathways was targeted through the concurrent inhibition of IR, ITGB1, and CD36 activity. A novel multicomponent MD simulation approach was employed to portray the simultaneous inhibition of IR, ITGB1, and CD36 by a 2:1 combination of Pimozide and Ponatinib. Further, in-vitro studies revealed the synergistic anticancer efficacy of drugs against monolayer as well as tumor spheroids of breast cancer cell lines (MCF-7 and MDA-MB-231). In addition, the combination therapy exerted approximately 40% of the apoptotic population and more than 1.5- to 3-fold reduction in the expression of ITGB1, IR, p-IR, IRS-1, and p-AKT in MCF-7 and MDA-MB-231 cell lines. Moreover, the reduction in fatty acid uptake, lipid droplet accumulation, cancer stemness, and migration properties were also observed. Thus, targeting IR, ITGB1, and CD36 in the interconnected network with the combination of Pimozide and Ponatinib represents a promising therapeutic approach for breast cancer.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"125 7","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140862478","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}