Biochimica et biophysica acta. Molecular cell research最新文献

{"title":"Hotspot mutant p53-R273H enhances mitochondrial biogenesis and cell migration in primary colorectal cancer in response to oxaliplatin","authors":"Toni Martinez-Bernabe ,&nbsp;Pere Miquel Morla-Barcelo ,&nbsp;Alessandra Fiore ,&nbsp;Massimo Donadelli ,&nbsp;Pilar Roca ,&nbsp;Jordi Oliver ,&nbsp;Jorge Sastre-Serra ,&nbsp;Daniel G. Pons","doi":"10.1016/j.bbamcr.2025.120073","DOIUrl":"10.1016/j.bbamcr.2025.120073","url":null,"abstract":"<div><div>Oxaliplatin is commonly known as a successful chemotherapy for advanced colorectal cancer, improving patient survival and eradicating micro-metastases, but its use in early stages remains controversial. Mitochondria fuel energy-intensive programs such as cell migration, yet how oxaliplatin regulates the mitochondrial network in CRC - and how <em>TP53</em> context shapes this - remains unclear. We investigated a matched pair of CRC cell lines from the same patient - SW480 (primary) and SW620 (lymph-node metastasis) - both harboring <em>TP53</em>-R273H mutation, to define differential responses in mitochondrial biogenesis, dynamics and respiration and the mechanisms underlying them. The results indicate that primary-derived colorectal cancer cell line increased cell migration, mitochondrial biogenesis, and mitochondrial respiration capacity in response to oxaliplatin through a new and firstly described gain-of-function (GOF) of p53-R273H. Additionally, in the primary-derived CRC line, oxaliplatin elicited fate heterogeneity - coexisting apoptotic and senescent fractions alongside an R273H-driven, bioenergetically primed migratory subpopulation - together with increased mitochondrial biogenesis and respiratory capacity; by contrast, the metastatic-derived line was more sensitive and displayed structural mitochondrial injury with reduced maximal respiration. More broadly, this work underscores the importance of p53 gain-of-function mutations in CRC: the same GOF (<em>TP53</em>-R273H) amplifies cell migration by coupling an enhanced mitochondrial biogenesis/OXPHOS program to motility. Oxaliplatin further accentuates this energetically primed, pre-metastatic state, arguing for mitochondrial-targeted combination strategies in early-stage CRC.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 1","pages":"Article 120073"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145399590","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cell-penetrant peptides as novel inhibitors of the interaction of coatomer protein COPB2/RACK2 with protein kinase Cε and cargo proteins","authors":"Abisola A. Olushola-Siedoks ,&nbsp;Lewin Small ,&nbsp;Kathryn J. Fincham ,&nbsp;Dorothy C.C. Wai ,&nbsp;Dhruv Monteiro ,&nbsp;James R.W. Conway ,&nbsp;Antonia Cadell ,&nbsp;Benjamin J. Parker ,&nbsp;David R. Croucher ,&nbsp;Carsten Schmitz-Peiffer ,&nbsp;Raymond S. Norton","doi":"10.1016/j.bbamcr.2025.120071","DOIUrl":"10.1016/j.bbamcr.2025.120071","url":null,"abstract":"<div><div>The lipid-activated novel protein kinase C isoform, PKCε, plays a key role in the progression of Type 2 Diabetes Mellitus (T2DM) and has also been implicated in cancer, cardiac hypertrophy, pain and anxiety. As the spatial regulation of PKCε activity is linked to its interaction with the Receptor for Activated C Kinase 2 (RACK2, also known as COPB2), blockade of this interaction has potential therapeutic benefits for the treatment of several pathologies. Using a proximity-based chemiluminescent assay to monitor the binding of lipid-activated PKCε to RACK2, we discovered inhibitory peptides derived from the PKCε sequence; pentapeptides with a KxKxx motif and a C-terminal carboxylate potently inhibited this interaction, whereas other short sequences containing cationic residues were less effective. An alanine scan of the KIKIC peptide showed that the two Lys residues and C-terminal carboxylate were the most important for inhibitory activity. A previously described PKCε translocation inhibitory peptide from PKCε, εV1-2, exhibited much weaker inhibition of the PKCe-RACK2 interaction, with significant inhibitory activity observed only when it was conjugated to cell-penetrating peptides. KIKIC exhibited moderate cell-penetrating ability, showed no evidence of cytotoxicity, and modified PKCε translocation in response to lipid treatment. Several proteins that were captured in a RACK2 pulldown of a liver lysate in a KIKIC-peptide sensitive manner were identified as part of a PKCε-RACK2 complex isolated from intact cells. These results provide a basis for the rational design of peptides or peptidomimetics that inhibit the PKCε-RACK2 interaction and have potential for the prevention and/or treatment of T2DM.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 1","pages":"Article 120071"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145336318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Canagliflozin inhibits p38MAPK signaling to protect tubular epithelial cell against pyroptosis in sepsis-induced acute kidney injury","authors":"Yun-feng Zhu ,&nbsp;Jing Wang ,&nbsp;Rong-xin Bian ,&nbsp;Chun-lin Guo ,&nbsp;Li-ge Song ,&nbsp;Chun-ying Nie ,&nbsp;Gang Liu","doi":"10.1016/j.bbamcr.2025.120069","DOIUrl":"10.1016/j.bbamcr.2025.120069","url":null,"abstract":"<div><div>This paper aimed to investigate the impacts and mechanisms of canagliflozin (CANA) in sepsis-induced acute kidney injury (SAKI). SAKI models were established using HK2 cells treated with lipopolysaccharide (LPS) and mice received cecum ligation puncture (CLP) surgery. The pathological examination was applied to evaluate mouse kidney damage. Inflammatory cytokines were evaluated using ELISA and RT-qPCR assay. Flow cytometry and TUNEL staining were employed to check cell apoptosis. The expression of apoptosis-, inflammation-, pyroptosis-, and pathway-related proteins were assessed via western blot. In CLP-induced mouse SAKI model, CANA attenuated renal pathological injury, inflammation response, pyroptosis and inhibited the p38MAPK pathway, as evidenced by the decrease of serum Scr and BUN levels, cell apoptosis, IL-1β and IL-18 levels, as well as GSDMD-N, cleaved caspase-1, and p38MAPK expression. In HK2 cells treated with LPS, inflammation response, pyroptosis, and the p38MAPK pathway were inhibited by CANA. Moreover, overexpression of p38MAPK reversed CANAs' effects on apoptosis, inflammation response, and pyroptosis in HK2 cells. In SAKI, CANA inhibited the p38MAPK pathway, thereby reducing cell apoptosis, inflammation response, and pyroptosis, which ultimately alleviating disease progression.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 1","pages":"Article 120069"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145290881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ATR-FTIR spectroscopy as a reliable analytical tool in cancer research: Tracking glycosylation-induced protein and lipid alteration in extracellular vesicles","authors":"Magdalena Wilczak ,&nbsp;Andrzej Wróbel ,&nbsp;Magdalena Surman ,&nbsp;Martyna Durak-Kozica ,&nbsp;Ewa Ł. Stępień ,&nbsp;Małgorzata Przybyło","doi":"10.1016/j.bbamcr.2025.120082","DOIUrl":"10.1016/j.bbamcr.2025.120082","url":null,"abstract":"<div><div>The rising incidence of cancer creates an urgent need to develop faster methods for early detection. Fourier Transform Infrared Spectroscopy (FTIR) spectroscopy is a promising technique to analyse molecular content in biological samples. FTIR has also been used to study structural changes in extracellular vesicles (EVs), revealing alterations in protein secondary structure, protein-to-lipid ratio, and protein phosphorylation levels. We investigated how changes in glycosylation, which naturally occur during tumor progression, affect the previously mentioned parameters and whether these cellular changes are reflected in EV composition. The WM266–4 melanoma cell line, treated with two glycosylation inhibitors, was used as a model. After treatment, EVs were isolated and ATR-FTIR measurements were performed, followed by a comprehensive analysis of the data. Significant differences in protein and lipid content were observed between EV populations treated with glycosylation inhibitors, with greater changes in EVs compared to cells. Glycosylation inhibitors also increased the level of phosphorylated proteins in EVs. Our findings showed that changes in EVs were more dynamic than at the cellular level cells. The presented analysis shows that subtle molecular changes can significantly impact EV cargo and properties. FTIR is a powerful tool for detecting these changes and may aid future cancer diagnostics.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 1","pages":"Article 120082"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145450692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glaucoma-associated polymorphism M98K-OPTN sensitizes retinal cells to protein homeostasis stress through p62-mediated caspase activation","authors":"Swetha Medchalmi,&nbsp;Zuberwasim Sayyad ,&nbsp;Ghanshyam Swarup","doi":"10.1016/j.bbamcr.2025.120064","DOIUrl":"10.1016/j.bbamcr.2025.120064","url":null,"abstract":"<div><div>M98K polymorphism of OPTN is significantly associated with glaucoma in certain populations. This raises the possibility that M98K-OPTN alone is not sufficient to cause glaucoma, and it may require cooperation with other genetic or environmental factors to induce glaucoma. Loss of vision in glaucoma occurs due to the degeneration of retinal ganglion cells. Here, we have tested the hypothesis that M98K-OPTN may enhance the sensitivity of retinal cells to protein homeostasis stress. For this purpose, we have used M98K-OPTN expressing and wild-type (WT)-OPTN expressing clones of retinal 661W cells. Upon induction of protein homeostasis stress by a proteasome inhibitor MG132 (1–2 μM), M98K-OPTN expressing cells showed reduced survival, and enhanced caspase-8, caspase-9, and caspase-3 activation in comparison with WT-OPTN expressing cells. Compared to WT-OPTN expressing cells, M98K-OPTN expressing cells showed enhanced formation of p62/SQSTM1-positive aggregates and enhanced p62 protein level under conditions of protein homeostasis stress. Knockdown of p62 resulted in reduced caspase-9, caspase-8, and caspase-3 activation in M98K-OPTN expressing cells treated with proteasome inhibitor. Our results suggest that M98K-OPTN modulates protein homeostasis stress-induced signalling that mediates p62-dependent caspase activation, which leads to enhanced sensitivity of M98K-OPTN expressing retinal cells to protein homeostasis stress.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 1","pages":"Article 120064"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145157204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transgenic overexpression of miR-486 and sAnk1.5 does not alter glucose handling in mice","authors":"S. Buonocore ,&nbsp;F. Fiore ,&nbsp;E.M. Rubino ,&nbsp;M.R. Catallo ,&nbsp;L. Raucci ,&nbsp;A. Laurino ,&nbsp;D. Rossi ,&nbsp;E. Pierantozzi ,&nbsp;V. Sorrentino","doi":"10.1016/j.bbamcr.2025.120087","DOIUrl":"10.1016/j.bbamcr.2025.120087","url":null,"abstract":"<div><div>Recent studies have shown that the C allele of SNP rs508419 is associated with susceptibility to Type 2 diabetes (T2D). This SNP lies within the muscle-specific P2 promoter of human ANK1, which drives transcription of the sAnk1.5 isoform and miR-486. The C allele increases P2 promoter activity, resulting to higher levels of sAnk1.5 transcript and protein in striated muscles.</div><div>We now present the first evidence that in skeletal muscle of individuals homozygous for the rs508419 C allele, also the hsa-miR-486-5p is transcribed at higher levels. This raises the question of whether T2D susceptibility may be associated with simultaneous overexpression of miR-486-5p and sAnk1.5. To test this hypothesis, we generated and characterized double transgenic (D-Tg) mice that selectively overexpress both mmu-miR-486-5p and sAnk1.5 in skeletal muscle tissue.</div><div>Analysis of sAnk1.5 and miR-486-5p expression in D-Tg mouse showed that despite both transgenes were significantly upregulated, a discrepancy between sAnk1.5 mRNA and protein levels was observed, suggesting that sAnk1.5 protein levels are further regulated by post-translational mechanism. D-Tg mice were monitored from 2 to 12 months of age to assess body weight, fat and lean mass, blood glucose levels under fasting conditions, as well as during intraperitoneal glucose tolerance tests and insulin tolerance tests, performed under either standard or high fat diet conditions. No differences were observed between D-Tg and age-matched wild type control mice for any of the parameters tested, indicating that the link between rs508419 and susceptibility to T2D cannot be ascribed to increased expression of miR-486-5p and sAnk1.5 in skeletal muscle.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 1","pages":"Article 120087"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145556246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Macrophage-derived FN1 promotes peritoneal cavity metastasis of gastric cancer by inhibiting the Hippo signaling pathway via SDC4","authors":"Meixia Zhang,&nbsp;Mingyan He,&nbsp;Fan Du,&nbsp;Yingping Xie,&nbsp;Ye Liao,&nbsp;Xiaolin Pan","doi":"10.1016/j.bbamcr.2025.120063","DOIUrl":"10.1016/j.bbamcr.2025.120063","url":null,"abstract":"<div><div>Gastric cancer (GC) is a prevalent malignant tumor worldwide. Peritoneal cavity metastasis is recognized as a critical clinical feature of late-stage GC. Fibronectin 1 (FN1) is closely associated with the development and progression of various cancers. This study aimed to investigate the functions of FN1 and the underlying mechanisms in peritoneal cavity metastasis of GC. A bioinformatics reanalysis of the single-cell sequencing dataset GSE140182 was performed to explore the cellular signature in malignant ascites. Cell communication analysis was performed to identify the cell communication between macrophages and tumor cells. GC cells were cultured with supernatant from FN1-overexpressing macrophages to investigate the effects and potential mechanism of FN1 action on GC cells by Western blot (WB) assay, MTT assay, migration and invasion assay, clone formation assay, cell adhesion assay, and functional rescue experiments. To further validate the impact of FN1 on GC and its peritoneal cavity metastasis were carried out in vivo experiments. Cellular communication between macrophages and GC cells was mediated by FN1-SDC4. Overexpression of macrophage-derived FN1 facilitated the malignant phenotypes of GC cells and the peritoneal cavity metastasis of GC in vivo. Mechanistically, macrophage-derived FN1 inhibited the Hippo signaling pathway by enhancing the expression of SDC4 in GC cells. Knockdown of SDC4 reversed the tumor-promoting effects induced by macrophage-derived FN1. Our study revealed that macrophage-derived FN1 inhibited the Hippo signaling pathway by upregulating the expression of SDC4 in GC cells, thereby promoting peritoneal cavity metastasis of GC.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 1","pages":"Article 120063"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145172856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"COA6 deficiency inhibits hepatocellular carcinoma progression by regulating cuproptosis through the JAK/STAT signaling pathway","authors":"Kailiang Tian ,&nbsp;Yang Yang ,&nbsp;Xiaohang Niu ,&nbsp;Xiaoming Wei ,&nbsp;Mingjin Zhang ,&nbsp;Yangliu Zhou ,&nbsp;Mingya Yang ,&nbsp;Haonan Sun ,&nbsp;Lixin Zhu ,&nbsp;Fubao Liu","doi":"10.1016/j.bbamcr.2025.120065","DOIUrl":"10.1016/j.bbamcr.2025.120065","url":null,"abstract":"<div><h3>Background</h3><div>Hepatocellular carcinoma (HCC) is one of the most common and deadly malignant tumors with limited therapeutic strategies. COA6 is a mitochondria-associated protein that plays an important role in regulating tumor cuproptosis, but its role in HCC is currently unknown. In this study, we aimed to investigate the expression and potential mechanism of action of COA6 in HCC.</div></div><div><h3>Methods</h3><div>TCGA-LIHC database was analyzed for differentially expressed cuproptosis-related genes (CRGs) in HCC and prognostic value, which was validated by immunohistochemistry and Western blot. CCK8, flow cytometry, wound healing, transwell and subcutaneous graft tumor assays were performed to explore the function of COA6 in HCC. Impact of COA6 on cuproptosis was assessed by assay kit and Western blot. RNA-sequencing were used to determine molecular mechanism. Immunoprecipitation (Co-IP) and immunofluorescence were used to assess the relationship between COA6 and NDUFA4L2. western blotting was used to detect the effect of COA6 on the JAK-STAT pathway.</div></div><div><h3>Results</h3><div>COA6 was significantly overexpressed in HCC tissues and HCC cell lines and was closely associated with poor prognosis. Silencing COA6 significantly inhibited the malignant phenotype of HUH7 and HepG2 cells in vitro and tumor growth in vivo. Moreover, silencing COA6 promoted ROS accumulation and activated cuproptosis in HCC cells. Interestingly, we found that COA6 interacted with NDUFA4L2 and COA6 deficiency significantly inhibited the JAK-STAT signaling pathway.</div></div><div><h3>Conclusions</h3><div>In conclusion, our data show that COA6 was highly expressed in HCC, and silencing COA6 blocked the JAK-STAT signaling pathway and activated cuproptosis, and inhibits the malignant phenotype and tumor growth of HCC cells. Therefore, targeting COA6 may be a potential therapeutic approach to inhibit HCC progression.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 1","pages":"Article 120065"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145181965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Plasma membrane Bile acid TGR5 receptor specific stimulation induces Ca2+ mobilisation, ATP secretion and P2Y receptors activation in cholangiocytes","authors":"Xuanmeng Chen ,&nbsp;Amr Al-Shebel ,&nbsp;Thibault Pebrier ,&nbsp;Thierry Tordjmann ,&nbsp;Olivier Dellis","doi":"10.1016/j.bbamcr.2025.120067","DOIUrl":"10.1016/j.bbamcr.2025.120067","url":null,"abstract":"<div><div>The Bile Acid receptor TGR5 is well known to activate the cAMP pathway leading to CFTR activation and Cl⁻ ions secretion, needed for bile alkalinization and hydration. However, during cystic fibrosis development, only 10 to 15 % of the patients present liver defects due to bile duct disorders, meaning that another process should compensate for the loss of CFTR activity. Interestingly, some bile acids had also been reported to mobilize Ca²⁺ ions in cholangiocytes. Using normal human cholangiocytes and cholangiocarcinoma cell lines, we confirmed by using a specific agonist, that TGR5 stimulation induced a Ca²⁺ release from the endoplasmic reticulum and an influx of extracellular Ca²⁺ ions. Next, this Ca²⁺ mobilisation allows an ATP (and UTP) release, leading to the activation of P2Y receptors, reinforcing this Ca²⁺ mobilisation. This study shows that activation of the BA receptor TGR5 has the capacity to induce the two main intracellular pathways, cAMP and IP₃-Ca²⁺ in cholangiocytes. From our data, we speculate that the pathway we described will allow activation of the Ca²⁺-activated Cl⁻ channels TMEM16A, to compensate in part or in totality the loss of CFTR in CF patients.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 1","pages":"Article 120067"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145211446","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"13th Tuscany Retreat on Cancer Research and Apoptosis: Genetic profiling, resistance mechanisms and novel treatment concepts in cancer and neurodegeneration","authors":"Femke Speelman-Rooms ,&nbsp;Olga Troitskaya ,&nbsp;Hannah Coxhead ,&nbsp;Claire Naveh ,&nbsp;Konstantinos Kelepouras ,&nbsp;Marta Manik ,&nbsp;Annalena Renner ,&nbsp;Dhairya Rajguru ,&nbsp;Jelena Budimir ,&nbsp;Fatma Isil Yapici ,&nbsp;Ophélie Champion","doi":"10.1016/j.bbamcr.2025.120079","DOIUrl":"10.1016/j.bbamcr.2025.120079","url":null,"abstract":"<div><div>The 13th edition of the Tuscany Retreat on Cancer Research and Apoptosis was convened on August 23rd to 30th, 2025, continuing its tradition as a biennial forum for scientific exchange. The Retreat brought together leading investigators focused on cancer biology, programmed cell death, and neurodegenerative disorders. Presentations and discussions encompassed diverse themes, including mechanisms of therapeutic resistance, advances in molecular signaling networks, and the identification of novel cellular targets. All topics were unified by their relevance to the regulation of programmed cell death and the pathological consequences of its disruption. Through this review, we intend to convey the essence of the scientific exchanges and to summarize the major take-home messages derived from the Retreat.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 1","pages":"Article 120079"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145421290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}