Journal of physiology and biochemistry最新文献_第7页

PGC-1α activation boosts exercise-dependent cellular response in the skeletal muscle. PGC-1α 激活可促进骨骼肌中依赖运动的细胞反应。

IF 3.4 3区生物学

Journal of physiology and biochemistry Pub Date : 2024-05-01 Epub Date: 2024-01-23 DOI: 10.1007/s13105-024-01006-1

Soroosh Mozaffaritabar, Erika Koltai, Lei Zhou, Zoltan Bori, Attila Kolonics, Sylwester Kujach, Yaodong Gu, Atsuko Koike, Anita Boros, Zsolt Radák

{"title":"PGC-1α activation boosts exercise-dependent cellular response in the skeletal muscle.","authors":"Soroosh Mozaffaritabar, Erika Koltai, Lei Zhou, Zoltan Bori, Attila Kolonics, Sylwester Kujach, Yaodong Gu, Atsuko Koike, Anita Boros, Zsolt Radák","doi":"10.1007/s13105-024-01006-1","DOIUrl":"10.1007/s13105-024-01006-1","url":null,"abstract":"The role of Peroxisome proliferator-activated receptor-gamma coactivator alpha (PGC-1α) in fat metabolism is not well known. In this study, we compared the mechanisms of muscle-specific PGC-1α overexpression and exercise-related adaptation-dependent fat metabolism. PGC-1α trained (PGC-1α Ex) and wild-trained (wt-ex) mice were trained for 10 weeks, five times a week at 30 min per day with 60 percent of their maximal running capacity. The PGC-1α overexpressed animals exhibited higher levels of Fibronectin type III domain-containing protein 5 (FNDC5), 5' adenosine monophosphate-activated protein kinase alpha (AMPK-α), the mammalian target of rapamycin (mTOR), Sirtuin 1 (SIRT1), Lon protease homolog 1 (LONP1), citrate synthase (CS), succinate dehydrogenase complex flavoprotein subunit A (SDHA), Mitofusin-1 (Mfn1), endothelial nitric oxide synthase (eNOS), Hormone-sensitive lipase (HSL), adipose triglyceride lipase (ATGL), G protein-coupled receptor 41 (GPR41), and Phosphatidylcholine Cytidylyltransferase 2 (PCYT2), and lower levels of Sirtuin 3 (SIRT3) compared to wild-type animals. Exercise training increased the protein content levels of SIRT1, HSL, and ATGL in both the wt-ex and PGC-1α trained groups. PGC-1α has a complex role in cellular signaling, including the upregulation of lipid metabolism-associated proteins. Our data reveals that although exercise training mimics the effects of PGC-1α overexpression, it incorporates some PGC-1α-independent adaptive mechanisms in fat uptake and cell signaling.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"329-335"},"PeriodicalIF":3.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11074013/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139521270","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}

引用次数: 0

Sorcin promotes proliferation of hepatocellular carcinoma by regulating VEGFA/B via PI3K pathway. Sorcin通过PI3K途径调节VEGFA/B，促进肝细胞癌的增殖。

IF 3.4 3区生物学

Journal of physiology and biochemistry Pub Date : 2024-05-01 Epub Date: 2024-03-27 DOI: 10.1007/s13105-024-01011-4

Huan Zhang, Shanshan Hu, Jaceline Gislaine Pires Sanches, Yizi Li, Yuanyi Wei, Chunwen Pu, Jun Zhang

引用次数: 0

The role of PKM2 in cancer progression and its structural and biological basis. PKM2 在癌症进展中的作用及其结构和生物学基础。

IF 3.4 3区生物学

Journal of physiology and biochemistry Pub Date : 2024-05-01 Epub Date: 2024-02-08 DOI: 10.1007/s13105-024-01007-0

Bingxin Wu, Zuhui Liang, Huan Lan, Xiaojun Teng, Caiyan Wang

{"title":"The role of PKM2 in cancer progression and its structural and biological basis.","authors":"Bingxin Wu, Zuhui Liang, Huan Lan, Xiaojun Teng, Caiyan Wang","doi":"10.1007/s13105-024-01007-0","DOIUrl":"10.1007/s13105-024-01007-0","url":null,"abstract":"Pyruvate kinase M2 (PKM2), a subtype of pyruvate kinase (PK), has been shown to play an important role in the development of cancer. It regulates the last step of glycolytic pathway. PKM2 has both pyruvate kinase and protein kinase activity, and the conversion of these two functions of PKM2 depends on the mutual change of dimer and tetramer. The dimerization of PKM2 can promote the proliferation and growth of tumor cells, so inhibiting the dimerization of PKM2 is essential to curing cancer. The aggregation of PKM2 is regulated by both endogenous and exogenous cofactors as well as post-translational modification (PTM). Although there are many studies on the different aggregation of PKM2 in the process of tumor development, there are few summaries in recent years. In this review, we first introduce the role of PKM2 in various biological processes of tumor growth. Then, we summarize the aggregation regulation mechanism of PKM2 by various endogenous cofactors such as Fructose-1, 6-diphosphate (FBP), various amino acids, and post-translational modification (PTMs). Finally, the related inhibitors and agonists of PKM2 are summarized to provide reference for regulating PKM2 aggregation in the treatment of cancer in the future.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"261-275"},"PeriodicalIF":3.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139702768","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}

引用次数: 0

Effect of chronic cold stress on gut microbial diversity, intestinal inflammation and pyroptosis in mice. 慢性冷应激对小鼠肠道微生物多样性、肠道炎症和热变态反应的影响

IF 3.4 3区生物学

Journal of physiology and biochemistry Pub Date : 2024-05-01 Epub Date: 2024-03-25 DOI: 10.1007/s13105-024-01019-w

Hongming Lv, Shijie Xia, Yuxi He, Chunyu Qiao, Jiahe Liu, Jingru Guo, Shize Li

{"title":"Effect of chronic cold stress on gut microbial diversity, intestinal inflammation and pyroptosis in mice.","authors":"Hongming Lv, Shijie Xia, Yuxi He, Chunyu Qiao, Jiahe Liu, Jingru Guo, Shize Li","doi":"10.1007/s13105-024-01019-w","DOIUrl":"10.1007/s13105-024-01019-w","url":null,"abstract":"Hypothermia is an essential environmental factor in gastrointestinal diseases, but the main molecular mechanisms of pathogenesis remain unclear. The current study sought to better understand how chronic cold stress affects gut damage and its underlying mechanisms. In this work, to establish chronic cold stress (CS)-induced intestinal injury model, mice were subjected to continuous cold exposure (4 °C) for 3 h per day for 3 weeks. Our results indicated that CS led to gut injury via inducing changes of heat shock proteins 70 (HSP70) and apoptosis-related (caspases-3, Bax and Bcl-2) proteins; enhancing expression of intestinal tight-related (ZO-1 and occludin) proteins; promoting releases of inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α), cyclooxygenase-2 (COX-2), high mobility group box 1 (HMGB1), interleukin1β (IL-1β), IL-18 and IL-6 inflammatory mediators in the ileum; and altering gut microbial diversity. Furthermore, persistent cold exposure resulted in the cleavage of pyroptosis-related Gasdermin D (GSDMD) protein by regulating the NLRP3/ASC/caspase-1 and caspase-11 pathway, and activation of toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)-mediated nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways, which are strongly associated with changes in gut microbiota diversity. Taken together, these investigations provide new insights into the increased risk of intestinal disorders at extremely low temperatures and establish a theoretical foundation for the advancement of novel pharmaceutical interventions targeting cold-related ailments.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"465-477"},"PeriodicalIF":3.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140288404","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}

引用次数: 0

Lactate ameliorates palmitate-induced impairment of differentiative capacity in C2C12 cells through the activation of voltage-gated calcium channels. 乳酸盐通过激活电压门控钙通道改善棕榈酸酯诱导的 C2C12 细胞分化能力损伤。

IF 3.4 3区生物学

Journal of physiology and biochemistry Pub Date : 2024-05-01 Epub Date: 2024-02-19 DOI: 10.1007/s13105-024-01009-y

Juan Wan, Chunfang Cheng, Xiaonuo Li, Yuanjie Zhu, Hu Su, Yanchun Gong, Kaizhi Ding, Xiaofei Gao, Caixia Dang, Guoyin Li, Wei Jiang, Li-Hua Yao

{"title":"Lactate ameliorates palmitate-induced impairment of differentiative capacity in C2C12 cells through the activation of voltage-gated calcium channels.","authors":"Juan Wan, Chunfang Cheng, Xiaonuo Li, Yuanjie Zhu, Hu Su, Yanchun Gong, Kaizhi Ding, Xiaofei Gao, Caixia Dang, Guoyin Li, Wei Jiang, Li-Hua Yao","doi":"10.1007/s13105-024-01009-y","DOIUrl":"10.1007/s13105-024-01009-y","url":null,"abstract":"Palmitic acid (PA), a saturated fatty acid enriched in high-fat diet, has been implicated in the development of skeletal muscle regeneration dysfunction. This study aimed to examine the effects and mechanisms of lactate (Lac) treatment on PA-induced impairment of C2C12 cell differentiation capacity. Furthermore, the involvement of voltage-gated calcium channels in this context was examined. In this study, Lac could improve the PA-induced impairment of differentiative capacity in C2C12 cells by affecting Myf5, MyoD and MyoG. In addition, Lac increases the inward flow of Ca2+, and promotes the depolarization of the cell membrane potential, thereby activating voltage-gated calcium channels during C2C12 cell differentiation. The enchancement of Lac on myoblast differentiative capacity was abolished after the addition of efonidipine (voltage-gated calcium channel inhibitors). Therefore, voltage-gated calcium channels play an important role in improving PA-induced skeletal muscle regeneration disorders by exercising blood Lac. Our study showed that Lac could rescue the PA-induced impairment of differentiative capacity in C2C12 cells by affecting Myf5, MyoD and MyoG through the activation of voltage-gated calcium channels.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"349-362"},"PeriodicalIF":3.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139900085","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}

引用次数: 0

Itaconate inhibits corticosterone-induced necroptosis and neuroinflammation via up-regulating menin in HT22 cells. 伊塔康酸通过上调 HT22 细胞中的 menin 抑制皮质酮诱导的坏死和神经炎症。

IF 3.4 3区生物学

Journal of physiology and biochemistry Pub Date : 2024-05-01 Epub Date: 2024-03-01 DOI: 10.1007/s13105-024-01012-3

Jin-Yu Liang, Shan Gao, Jia-Mei Jiang, Pin Zhang, Wei Zou, Xiao-Qing Tang, Yi-Yun Tang

{"title":"Itaconate inhibits corticosterone-induced necroptosis and neuroinflammation via up-regulating menin in HT22 cells.","authors":"Jin-Yu Liang, Shan Gao, Jia-Mei Jiang, Pin Zhang, Wei Zou, Xiao-Qing Tang, Yi-Yun Tang","doi":"10.1007/s13105-024-01012-3","DOIUrl":"10.1007/s13105-024-01012-3","url":null,"abstract":"Corticosterone (CORT) damages hippocampal neurons as well as induces neuroinflammation. The tricarboxylic acid cycle metabolite itaconate has an anti-inflammatory role. Necroptosis is a form of programmed cell death, also known as inflammatory cell death. Menin is a multifunctional scaffold protein, which deficiency aggravates neuroinflammation. In this study, we explored whether itaconate inhibits CORT-induced neuroinflammation as well as necroptosis and further investigated the mediatory role of Menin in this protective effect of itaconate by using an exposure of CORT to HT22 cells (a hippocampal neuronal cell line). The viability of HT22 cells was examined by the cell counting kit 8 (CCK-8). The morphology of HT22 cells was observed by transmission electron microscope (TEM). The expressions of necroptosis-related proteins (p-RIP1/RIP1, p-RIP3/RIP3, and p-MLKL/MLKL) were evaluated by western blotting. The contents of inflammatory factors were detected by an enzyme-linked immunosorbent assay (ELISA) kit. Our results showed that CORT increases the contents of pro-inflammatory factors (IL-1β, TNF-α) as well as decreases the contents of anti-inflammatory factors (IL-4, IL-10) in HT22 cells. We also found that CORT increases the expressions of necroptosis-related proteins (p-RIP1/RIP1, p-RIP3/RIP3, and p-MLKL/MLKL) and decreases the cell viability in HT22 cells, indicating that CORT induces necroptosis in HT22 cells. Itaconate improves CORT-induced neuroinflammation and necroptosis. Furthermore, itaconate upregulates the expression of Menin in CORT-exposed HT22 cells. Importantly, silencing Menin abolishes the antagonistic effect of itaconate on CORT-induced necroptosis and neuroinflammation. In brief, these results indicated that itaconate protects HT22 cells against CORT-induced neuroinflammation and necroptosis via upregulating Menin.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"393-405"},"PeriodicalIF":3.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139996550","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}

引用次数: 0

An experimental model of western diet in female Wistar rats leads to cardiac hypoxia related to a stimulated contractility. 雌性 Wistar 大鼠的西式饮食实验模型会导致心脏缺氧，这与刺激收缩力有关。

IF 3.4 3区生物学

Journal of physiology and biochemistry Pub Date : 2024-05-01 Epub Date: 2024-01-04 DOI: 10.1007/s13105-023-01003-w

Jean-Paul Rigaudière, Chrystèle Jouve, Frédéric Capel, Véronique Patrac, Bruno Miguel, Anne Tournadre, Luc Demaison

{"title":"An experimental model of western diet in female Wistar rats leads to cardiac hypoxia related to a stimulated contractility.","authors":"Jean-Paul Rigaudière, Chrystèle Jouve, Frédéric Capel, Véronique Patrac, Bruno Miguel, Anne Tournadre, Luc Demaison","doi":"10.1007/s13105-023-01003-w","DOIUrl":"10.1007/s13105-023-01003-w","url":null,"abstract":"Previous studies in Western diet (WD)-fed male rats have highlighted a link between the stimulation of cardiac contractility, mitochondrial adaptations and a pro-inflammatory fatty acid profile of phospholipids in the heart. Our objectives were to determine (1) if WD-fed female Wistar rats and obese humans display a similar pro-inflammatory profile in their cardiac phospholipids and (2) if this lipid profile is associated with deleterious effects on the heart of the female rodents. Female Wistar rats were fed WD for 5 weeks or a laboratory chow as a control. Ionic homeostasis, redox status, inflammation markers, and fatty acid composition of phospholipids were analysed in the heart. WD increased the abdominal fat mass without modifying the body weight of female rats. As previously found in males, a WD induced a shift in membrane fatty acid composition toward a pro-inflammatory profile in the female rats, but not in obese humans. It was associated with an increased COX2 expression suggesting an increased pro-inflammatory eicosanoid production. Signs of increased intracellular calcium strongly supported a stimulation of cardiac contractility without any induction of apoptosis. The heart of WD-fed rats exhibited a hypoxic state as a higher HIF1-α expression was reported. The expressions of antioxidant enzymes were increased, but the redox reserves against reactive oxygen species were lowered. In conclusion, as previously observed in males, we suppose that cardiac abnormalities are magnified with severe obesity in female rats, leading to hypoxia and intense oxidative stress which could ultimately induce cell death and heart failure.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"287-302"},"PeriodicalIF":3.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139087317","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}

引用次数: 0

Lactate coordinated with exercise promoted the browning of inguinal white adipose tissue. 乳酸盐与运动的协调促进了腹股沟白色脂肪组织的棕色化。

IF 3.4 3区生物学

Journal of physiology and biochemistry Pub Date : 2024-05-01 Epub Date: 2024-01-04 DOI: 10.1007/s13105-023-01004-9

Xuefei Chen, Yanjun Li, Jingbo Zhang, Wenhua Huang, Jie Su, Jing Zhang

{"title":"Lactate coordinated with exercise promoted the browning of inguinal white adipose tissue.","authors":"Xuefei Chen, Yanjun Li, Jingbo Zhang, Wenhua Huang, Jie Su, Jing Zhang","doi":"10.1007/s13105-023-01004-9","DOIUrl":"10.1007/s13105-023-01004-9","url":null,"abstract":"Lactate, an important exercise metabolite, induces white adipose tissue browning by upregulated uncoupling protein 1 (UCP1) expression. However, the function of lactate during browning of inguinal white adipose tissue (iWAT) caused by exercise is unclear. Here, we considered lactate as an exercise supplement and investigated the effects of chronic pre-exercise lactate administration on energy metabolism and adipose tissue browning. C57B/L6 male mice (5 weeks of age) were divided into six groups. We evaluated the changes in blood lactate levels in each group of mice after the intervention. Energy expenditure was measured after the intervention immediately by indirect calorimetry. The marker protein levels and gene expressions were determined by western-blot and quantitative real-time PCR. HIIT significantly decreased adipose tissue weight while increased energy expenditure and the expression of UCP1 in iWAT; however, these regulations were inhibited in the DCA+HIIT group. Compared with the MICT and LAC groups, long-term lactate injection before MICT led to lower WAT weight to body weight ratios and higher energy expenditure in mice. Furthermore, the marker genes of browning in iWAT, such as Ucp1 and Pparγ, were significantly increased in the LAC+MICT group than in the other groups, and the expression of monocarboxylate transporter-1 (Mct1) mRNA was also significantly increased. Lactate was involved in exercise-mediated browning of iWAT, and its mechanism might be the increased of lactate transport through MCT1 or PPARγ upregulation induced by exercise. These findings suggest exogenous lactate may be a new exercise supplement to regulate metabolism.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"303-315"},"PeriodicalIF":3.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139087319","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}

引用次数: 0

NCS-1 protein regulates TRPA1 channel through the PI3K pathway in breast cancer and neuronal cells. NCS-1 蛋白通过 PI3K 途径调节乳腺癌和神经细胞中的 TRPA1 通道。

IF 3.4 3区生物学

Journal of physiology and biochemistry Pub Date : 2024-05-01 Epub Date: 2024-04-02 DOI: 10.1007/s13105-024-01016-z

Julio C Sánchez, Alexander Alemán, Juan F Henao, Juan C Olaya, Barbara E Ehrlich

{"title":"NCS-1 protein regulates TRPA1 channel through the PI3K pathway in breast cancer and neuronal cells.","authors":"Julio C Sánchez, Alexander Alemán, Juan F Henao, Juan C Olaya, Barbara E Ehrlich","doi":"10.1007/s13105-024-01016-z","DOIUrl":"10.1007/s13105-024-01016-z","url":null,"abstract":"The physical and functional interaction between transient receptor potential channel ankyrin 1 (TRPA1) and neuronal calcium sensor 1 (NCS-1) was assessed. NCS-1 is a calcium (Ca2+) sensor found in many tissues, primarily neurons, and TRPA1 is a Ca2+ channel involved not only in thermal and pain sensation but also in conditions such as cancer and chemotherapy-induced peripheral neuropathy, in which NCS-1 is also a regulatory component.We explored the interactions between these two proteins by employing western blot, qRT-PCR, co-immunoprecipitation, Ca2+ transient monitoring with Fura-2 spectrophotometry, and electrophysiology assays in breast cancer cells (MDA-MB-231) with different levels of NCS-1 expression and neuroblastoma cells (SH-SY5Y).Our findings showed that the expression of TRPA1 was directly correlated with NCS-1 levels at both the protein and mRNA levels. Additionally, we found a physical and functional association between these two proteins. Physically, the NCS-1 and TRPA1 co-immunoprecipitate. Functionally, NCS-1 enhanced TRPA1-dependent Ca2+ influx, current density, open probability, and conductance, where the functional effects depended on PI3K. Conclusion: NCS-1 appears to act not only as a Ca2+ sensor but also modulates TRPA1 protein expression and channel function in a direct fashion through the PI3K pathway. These results contribute to understanding how Ca2+ homeostasis is regulated and provides a mechanism underlying conditions where Ca2+ dynamics are compromised, including breast cancer. With a cellular pathway identified, targeted treatments can be developed for breast cancer and neuropathy, among other related diseases.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"451-463"},"PeriodicalIF":3.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11074019/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140336080","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}

引用次数: 0

Integrated clinical and prognostic analyses of mTOR/Hippo pathway core genes in hepatocellular carcinoma. 肝细胞癌中 mTOR/Hippo 通路核心基因的临床和预后综合分析。

IF 3.7 3区生物学

Journal of physiology and biochemistry Pub Date : 2024-05-01 Epub Date: 2024-03-12 DOI: 10.1007/s13105-024-01015-0

Tianhang Feng, Ping Chen, Tao Wang, Chunyou Lai, Yutong Yao

{"title":"Integrated clinical and prognostic analyses of mTOR/Hippo pathway core genes in hepatocellular carcinoma.","authors":"Tianhang Feng, Ping Chen, Tao Wang, Chunyou Lai, Yutong Yao","doi":"10.1007/s13105-024-01015-0","DOIUrl":"10.1007/s13105-024-01015-0","url":null,"abstract":"Hepatocellular carcinoma (HCC) is one of the most aggressive and dismal cancers globally. Emerging evidence has established that mTOR and Hippo pathways are oncogenic drivers of HCC. However, the prognostic value of these pathways in HCC remains unclear. In this study, we aimed to develop a gene signature utilizing the mTOR/Hippo genes for HCC prognostication. A multiple stage strategy was employed to screen, and a 12-gene signature based on mTOR/Hippo pathways was constructed to predict the prognosis of HCC patients. The risk scores calculated by the signature were inversely correlated with patient prognosis. Validation of the signature in independent cohort confirmed its predictive power. Further analysis revealed molecular differences between high and low-risk groups at genomic, transcriptomic, and protein-interactive levels. Moreover, immune infiltration analysis revealed an immunosuppressive state in the high-risk group. Finally, the gene signature could predict the sensitivity to current chemotherapeutic drugs. This study demonstrated that combinatorial mTOR/Hippo gene signature was a robust and independent prognostic tool for survival prediction of HCC. Our findings not only provide novel insights for the molecular understandings of mTOR/Hippo pathways in HCC, but also have important clinical implications for guiding therapeutic strategies.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"439-449"},"PeriodicalIF":3.7,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11074052/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140101850","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}

引用次数: 0