Cell Biochemistry and Biophysics最新文献_第2页

TOP2A Promotes Proliferation, Migration, and Inflammatory Response in M5-Treated Keratinocytes by Binding CTBP1 to Activate Wnt/β-Catenin Signaling. TOP2A 通过结合 CTBP1 激活 Wnt/β-Catenin 信号，促进经 M5 处理的角质形成细胞的增殖、迁移和炎症反应。

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-06-01 Epub Date: 2024-11-20 DOI: 10.1007/s12013-024-01620-2

Yuanwen Yang, Shumei Liu, Xia Xiao

{"title":"TOP2A Promotes Proliferation, Migration, and Inflammatory Response in M5-Treated Keratinocytes by Binding CTBP1 to Activate Wnt/β-Catenin Signaling.","authors":"Yuanwen Yang, Shumei Liu, Xia Xiao","doi":"10.1007/s12013-024-01620-2","DOIUrl":"10.1007/s12013-024-01620-2","url":null,"abstract":"Psoriasis is a chronic cutaneous disease, affecting a significant portion of the global population. Topoisomerase II alpha (TOP2A) is upregulated in psoriasis samples, but the precise molecular mechanism remains unclear. We aimed to clarify the biological contribution of TOP2A in psoriasis progression. An in vitro psoriasis model was established on M5-induced keratinocytes (HaCaT cells) to simulate the psoriasis-like alterations. Following TOP2A knockdown without or with c terminal binding protein 1 (CTBP1) overexpression, CCK-8 and EDU staining were employed to analyze the viability and proliferation of HaCaT cells under M5 conditions. The capacities of HaCaT cell migration and invasion were examined with wound healing- and transwell assays. RT-qPCR and immunoblotting were adopted for evaluation of the inflammation and differentiation of M5-stimualted HaCaT cells. Additionally, the binding between TOP2A and CTBP1 was predicated using bioinformatics tools and detected by Co-IP. Finally, the expression of proteins in Wnt/β-catenin signaling was analyzed with the application of immunoblotting. Results suggested that TOP2A was upregulated in psoriasis skin lesions and M5-induced HaCaT cells. Interference with TOP2A attenuated the proliferation, migration, invasion, and inflammatory response in M5-treated HaCaT cells. In particular, TOP2A bound to CTBP1 and upregulated CTBP1 expression in HaCaT cells. Remarkably, CTBP1 upregulation blocked the impacts of TOP2A depletion on the biological behaviors of M5-treated HaCaT cells. Besides, TOP2A deficiency upregulated DKK1 expression as well as downregulated Wnt1, β-catenin, and c-Myc expression in HaCaT cells exposed to M5, which was restored by further CTBP1 overexpression. In summary, TOP2A binds CTBP1 to activate Wnt/β-catenin signaling, thereby promoting the progression of psoriasis.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"2101-2113"},"PeriodicalIF":1.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142674491","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

HIF-3α Facilitates the Proliferation and Migration in Pancreatic Cancer by Inhibiting Autophagy Through Downregulating TP53INP2. HIF-3α通过下调TP53INP2抑制自噬促进胰腺癌细胞增殖和迁移

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-06-01 Epub Date: 2024-11-30 DOI: 10.1007/s12013-024-01624-y

Xianfei Zhou, Yisheng Ling, Luoshun Huang, Fan Yang, Yang Zhang, Yong Lan

{"title":"HIF-3α Facilitates the Proliferation and Migration in Pancreatic Cancer by Inhibiting Autophagy Through Downregulating TP53INP2.","authors":"Xianfei Zhou, Yisheng Ling, Luoshun Huang, Fan Yang, Yang Zhang, Yong Lan","doi":"10.1007/s12013-024-01624-y","DOIUrl":"10.1007/s12013-024-01624-y","url":null,"abstract":"Pancreatic cancer is a highly aggressive malignant tumor, often diagnosed late, leading to a poor prognosis and extremely high mortality rates. In recent years, the role of cellular autophagy in tumors has become increasingly prominent, gradually becoming an important target for malignant tumors. HIF-3α is a member of HIF family with potential oncogenic function. However, the role of HIF-3α in pancreatic cancer is not clear. The present study revealed its role in pancreatic cancer by exploring the regulatory mechanism of HIF-3α on autophagy. HIF-3α was found markedly upregulated in pancreatic cancer cell lines. In HIF-3α silenced MiaPaCa-2 cells, largely declined migration distance, reduced number of invaded cells and colonies, increased number of autophagosome, downregulated p62, and upregulated Beclin1, LC3II/I, and ATG7 were observed, accompanied by elevated TP53INP2 expressions. on the contrary, in HIF-3α overexpressed PANC-1 cells, notably increased migration distance, and elevated number of invaded cells and colonies were observed, along with decreased autophagosome, upregulated p62, and downregulated Beclin1, LC3II/I, ATG7, and TP53INP2. Subsequently, HIF-3α overexpressed PANC-1 cells were transfected with TP53INP2 overexpressing vector. The influence of HIF-3α overexpression on the proliferation, migration, invasion, and autophagy was abolished by TP53INP2 overexpressing. Furthermore, HIF-3α overexpression facilitated the in vivo growth of PANC-1 cells, accompanied by the autophagy inhibition in tumor tissues, which were remarkably abolished by TP53INP2 overexpressing. Collectively, HIF-3α facilitated the proliferation and migration in pancreatic cancer by inhibiting autophagy through downregulating TP53INP2.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"2139-2150"},"PeriodicalIF":1.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142764763","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Apatinib Mesylate Inhibits Cell Proliferation and the Metastasis of Esophageal Squamous Cell Carcinoma Through ERK/ELK-1/Snail Pathway. 甲磺酸阿帕替尼通过ERK/ELK-1/蜗牛通路抑制食管鳞状细胞癌细胞增殖和转移

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-06-01 Epub Date: 2024-12-21 DOI: 10.1007/s12013-024-01631-z

Xiang Feng, Di Xu, Zhuqin Xing, Qian Zhang

{"title":"Apatinib Mesylate Inhibits Cell Proliferation and the Metastasis of Esophageal Squamous Cell Carcinoma Through ERK/ELK-1/Snail Pathway.","authors":"Xiang Feng, Di Xu, Zhuqin Xing, Qian Zhang","doi":"10.1007/s12013-024-01631-z","DOIUrl":"10.1007/s12013-024-01631-z","url":null,"abstract":"This study aimed to evaluate the impact of apatinib (APT) mesylate on the growth, migration ability, and underlying mechanisms in esophageal squamous cell carcinoma (ESCC) cell lines Kyse30 and Kyse150. Additionally, the anti-metastatic effects of APT mesylate were further validated in a nude mouse xenograft metastasis model. In vitro, APT mesylate treatment significantly reduced cell viability and migration ability in both cell lines in a dose- and time-dependent manner. Western blot analysis showed that APT mesylate inhibited the expression of proteins involved in the ERK/ELK-1/Snail signaling pathway, including ERK1/2, Snail, N-cadherin, and Vimentin, while upregulating E-cadherin expression. In vivo, APT mesylate administration notably decreased the number of pulmonary metastatic nodules in nude mice, with higher doses showing more pronounced effects. The 200 mg/kg high-dose group exhibited a significantly lower number of metastatic nodules compared to the cisplatin (CIS) group. The results suggest that APT mesylate inhibits ESCC cell proliferation and migration primarily by suppressing the ERK/ELK-1/Snail signaling pathway, which mediates epithelial-mesenchymal transition (EMT) and reduces metastasis and invasiveness. This study provides experimental evidence for the potential clinical application of APT mesylate in targeted therapy for ESCC, indicating its promising clinical value.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"2201-2211"},"PeriodicalIF":1.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142871023","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Berberine and Cyperus rotundus extract nanoformulations protect the rats against Staphylococcus-induced mastitis via antioxidant and anti-inflammatory activities: role of MAPK signaling. 小檗碱和圆草提取物纳米配方通过抗氧化和抗炎活性保护大鼠免受葡萄球菌诱导的乳腺炎：MAPK信号的作用。

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-06-01 Epub Date: 2024-12-21 DOI: 10.1007/s12013-024-01628-8

Hanan A Edres, Ingi H Elmassry, Mohamed A Lebda, Sarah I Othman, Dina R S Gad El-Karim, Hassan A Rudayni, Sawsan Kh M Ebied, Ahmed A Allam, Aml E Hashem

{"title":"Berberine and Cyperus rotundus extract nanoformulations protect the rats against Staphylococcus-induced mastitis via antioxidant and anti-inflammatory activities: role of MAPK signaling.","authors":"Hanan A Edres, Ingi H Elmassry, Mohamed A Lebda, Sarah I Othman, Dina R S Gad El-Karim, Hassan A Rudayni, Sawsan Kh M Ebied, Ahmed A Allam, Aml E Hashem","doi":"10.1007/s12013-024-01628-8","DOIUrl":"10.1007/s12013-024-01628-8","url":null,"abstract":"Berberine (BER) and Cyperus rotundus rhizomes extract (CRE) are phytochemicals characterized by broad-spectrum pharmacological activity that could tackle the side effects of conventional mastitis therapies, however, they undergo a modest bioavailability. In the current study, nanoformulations of BER and CRE chitosan hydrogel (BER/CH-NPs, CRE/CH-NPs) were investigated for their antibacterial, antioxidant, anti-inflammatory and anti-apoptotic effects against S. aureus-induced mastitis in a rat model. The experiment was conducted on 80 early lactating female albino rats allocated into 6 groups; control, mastitis, BER/CH-NPs (1 and 0.5 mg), CRE/CH-NPs (0.5 and 0.25 mg), BER/CH-NPs + CRE/CH-NPs (0.5 + 0.25 and 0.25 + 0.125 mg). The nanoparticles were given by oral gavage once every other day from day 2 to day 12 after parturition. On the 13th day, intra-mammary inoculation with 100 µl of S. aureus suspension containing 2.1 × 108 CFU/ml in all groups except the control group. The results expressed the effect of BER/CH-NPs and CRE/CH-NPs on mammary gland tissue including significantly diminished viable bacterial load as well as attenuated the levels of MPO, MDA, caspase-3 with elevating Nrf2 level, and modulating glutathione redox. Also, the nanoformulations resulted in attenuation of the mRNA expression of TLR2, NOD2, Keap-1 and MAPK signaling pathway additional to the immune reactivity of NF-κB P65 and p-ERK as well as the preservation of the regular alveolar architecture. The supplementation of the berberine and Cyperus rotundus extract nanoformulations could be a prospective protective approach against Staphylococcal mastitis via their antibacterial, antioxidant, antiapoptotic, anti-inflammatory and modulation of MAPK signaling pathway.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"2167-2183"},"PeriodicalIF":1.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142871024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Interaction Between Allopregnanolone and Amiloride Binding Sites on the GABA_A Receptor. GABAA受体上异孕酮与阿米洛利结合位点的相互作用。

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-06-01 Epub Date: 2024-12-28 DOI: 10.1007/s12013-024-01654-6

Julia V Bukanova, Rodion V Kondratenko, Elena I Solntseva

{"title":"Interaction Between Allopregnanolone and Amiloride Binding Sites on the GABAA Receptor.","authors":"Julia V Bukanova, Rodion V Kondratenko, Elena I Solntseva","doi":"10.1007/s12013-024-01654-6","DOIUrl":"10.1007/s12013-024-01654-6","url":null,"abstract":"Allopregnanolone (Allo) is a positive allosteric modulator of the GABAA receptor, and amiloride (Ami) is a competitive antagonist of the GABAA receptor. The purpose of this work was to study the combined effect of Allo and Ami on functional activity of GABAA receptor. The GABA-induced chloride current (IGABA) was measured in isolated Purkinje cells of rat cerebellum using the patch-clamp technique and a system of fast application. Our results indicate that Allo suppresses the inhibitory effect of Ami on IGABA, the IC50 value of Ami concentration-response curve was increased from 164 to 547 µM (P < 0.001) in the presence of Allo. Next, GABA concentration-response curves (EC50 = 5.8 µM) were constructed in the presence of Allo (EC50 = 1.2 µM), Ami (EC50 = 25.5 µM), and the combination of Allo+Ami (EC50 = 3.2 µM). Changes in EC50 values as a percentage relative to the control were calculated. The blocking effect of Ami is reduced in the presence of Allo (340% vs 150%, P < 0.01) and the potentiating effect of Allo does not change in the presence of Ami (78% vs 87%, P > 0.05). The results suggest that there is an allosteric relationship between the Allo and Ami binding sites on GABAA receptor that operates in one direction, from Allo sites to Ami site, but not vice versa.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"2453-2459"},"PeriodicalIF":1.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142891190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Sudachitin Reduces Inflammatory Mediator Expression in Toll-Like Receptor 2 Ligand-Stimulated Human Dental Pulp Cells. Sudachitin减少toll样受体2配体刺激的人牙髓细胞中炎症介质的表达。

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-06-01 Epub Date: 2024-12-30 DOI: 10.1007/s12013-024-01652-8

Katsuhiro Mieda, Tadashi Nakanishi, Hitomi Kuramoto, Yoshitaka Hosokawa, Ikuko Hosokawa, Daisuke Takegawa, Keiichi Hosaka

{"title":"Sudachitin Reduces Inflammatory Mediator Expression in Toll-Like Receptor 2 Ligand-Stimulated Human Dental Pulp Cells.","authors":"Katsuhiro Mieda, Tadashi Nakanishi, Hitomi Kuramoto, Yoshitaka Hosokawa, Ikuko Hosokawa, Daisuke Takegawa, Keiichi Hosaka","doi":"10.1007/s12013-024-01652-8","DOIUrl":"10.1007/s12013-024-01652-8","url":null,"abstract":"Sudachitin, which is a polymethoxy flavonoid derived from the peer of Citrus sudachi, has several biological properties. However, the effect of sudachitin on human dental pulp cells (HDPCs) remains unclear. The aim of this study was to investigate whether sudachitin could decrease the expression of inflammatory mediators such as cytokines and prostaglandin in HDPCs stimulated with Pam3CSK4, a ligand for toll-like receptor (TLR) 2. HDPCs were pre-incubated with different concentrations of sudachitin (6.25, 12.5, 25, or 50 μM) and stimulated with Pam3CSK4 (100 ng/mL). The quantification of inflammatory cytokines (interleukin (IL)-6, IL-8, and C-X-C motif chemokine ligand (CXCL) 10) and prostaglandin E2 (PGE2) were performed by enzyme-linked immunosorbent assay (ELISA). The expression of cyclooxygenase (COX)-2, a key enzyme for PGE2 formation, was analyzed by western blot. Moreover, the activations of cell signal pathways were examined by western blot analysis. Sudachitin suppressed IL-6, IL-8, CXCL10, and PGE2 production and COX-2 protein expression in Pam3CSK4-stimulated HDPCs. In addition, we revealed that nuclear factor-kappa B (NF-κB) and protein kinase B (Akt) pathways in the Pam3CSK4-stimulated HDPCs were inhibited by sudachitin treatment. These findings suggest that sudachitin can reduce inflammatory mediator production in HDPCs stimulated with TLR2 ligand by inhibiting NF-κB and Akt activations.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"2431-2439"},"PeriodicalIF":1.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142908934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Synephrine Inhibits Oxidative Stress and H₂O₂-Induced Premature Senescence. 辛弗林抑制氧化应激和h2o2诱导的过早衰老。

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-06-01 Epub Date: 2025-01-20 DOI: 10.1007/s12013-025-01669-7

Hiroshi Abe, Hiroko P Indo, Hiromu Ito, Hideyuki J Majima, Tatsuro Tanaka

{"title":"Synephrine Inhibits Oxidative Stress and H2O2-Induced Premature Senescence.","authors":"Hiroshi Abe, Hiroko P Indo, Hiromu Ito, Hideyuki J Majima, Tatsuro Tanaka","doi":"10.1007/s12013-025-01669-7","DOIUrl":"10.1007/s12013-025-01669-7","url":null,"abstract":"Synephrine, a protoalkaloid found in Citrus aurantium (CA) peels, exerts lipolytic, anti-inflammatory, and vasoconstrictive effects; however, its antioxidant activity remains unclear. In this study, electron spin resonance spectroscopy revealed that synephrine scavenged both hydroxyl and superoxide anion radicals. Several external stimuli, such as H2O2, X-rays, and ultraviolet (UV) radiation, cause stress-induced premature senescence (SIPS). As oxidative stress induces SIPS, we hypothesized that synephrine, an antioxidant, would suppress H2O2-induced premature senescence in WI-38 cells. Synephrine significantly decreased the reactive oxygen species levels induced by H2O2, thereby reducing lipid peroxidation, and oxidative DNA damage and preventing SIPS. Additionally, synephrine inhibited mitochondrial dysfunction in H2O2-treated WI-38 cells. The expression levels of p53, p21, and p16-INK4A, which are involved in the induction of cell cycle arrest in SIPS, were significantly lower in synephrine-treated cells than in untreated cells. Our results indicate that synephrine inhibits H2O2-induced oxidative stress and mitochondrial dysfunction, suppressing premature senescence by inhibiting activation of the p53-p21 and p16-INK4A-pRB pathways.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"2607-2622"},"PeriodicalIF":1.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12089197/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142998169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

MICAL1 Mediates TGF-β1-Induced Epithelial-to-Mesenchymal Transition and Metastasis of Hepatocellular Carcinoma by Activating Smad2/3. MICAL1通过激活Smad2/3介导TGF-β1诱导的肝癌上皮-间质转化和转移。

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-06-01 Epub Date: 2025-02-15 DOI: 10.1007/s12013-025-01668-8

Xun Zhuang, Chunrong Wang, Zhenghui Ge, Mengjie Wu, Mengjiao Chen, Zhen Chen, Jianghong Hu

{"title":"MICAL1 Mediates TGF-β1-Induced Epithelial-to-Mesenchymal Transition and Metastasis of Hepatocellular Carcinoma by Activating Smad2/3.","authors":"Xun Zhuang, Chunrong Wang, Zhenghui Ge, Mengjie Wu, Mengjiao Chen, Zhen Chen, Jianghong Hu","doi":"10.1007/s12013-025-01668-8","DOIUrl":"10.1007/s12013-025-01668-8","url":null,"abstract":"Epithelial-mesenchymal transition (EMT) induced by transforming growth factor-β (TGF-β) is involved in hepatocellular carcinoma (HCC) growth and metastasis. Our study aimed to investigate the role of molecules interacting with CasL 1 (MICAL1) in regulating TGF-β-triggered EMT in HCC and the related mechanisms. After detecting MICAL1 expression and prognostic value in HCC, in vitro assays including CCK-8 assay, EdU staining, flow cytometry assay, Transwell assay, western blotting, and RT-qPCR and in vivo metastasis assay was conducted to evaluate the influence of MICAL1 knockdown on the proliferation and apoptosis as well as TGF-β-induced EMT and metastasis of Huh7 and MHCC97H cells. MICAL1 was highly expressed in HCC, and its high expression was related to histological grade, TNM stage, and shorter overall survival of HCC patients. MICAL1 silencing suppressed proliferation, promoted apoptosis, and curbed TGF-β1-triggered cytoskeletal remodeling, EMT, and metastasis of HCC cells. MICAL1 knockdown impeded TGF-β1-induced upregulation in phosphorylated-Smad2/3 protein levels and reduced Smad2/3 mRNA levels in HCC cells. MICAL1 downregulation enhanced the polyubiquitination and proteasomal degradation of TβRI. Additionally, MICAL1 silencing suppressed tumor growth and lung metastasis in Huh7-derived xenograft mouse models. Collectively, MICAL1 knockdown impairs TGF-β1-stimulated EMT and metastasis of HCC cells by restraining Smad2/3 phosphorylation and activation.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"2589-2606"},"PeriodicalIF":1.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143424612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Phellodendrine Exerts Protective Effects on Intra-abdominal Sepsis by Inactivating AKT/NF-kB Signaling. 黄柏碱通过抑制AKT/NF-kB信号通路对腹腔脓毒症的保护作用

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-06-01 Epub Date: 2025-02-14 DOI: 10.1007/s12013-024-01658-2

Ang Li, Peng Liu, Jiaohong Gan, Weijun Fang, Anjie Liu

{"title":"Phellodendrine Exerts Protective Effects on Intra-abdominal Sepsis by Inactivating AKT/NF-kB Signaling.","authors":"Ang Li, Peng Liu, Jiaohong Gan, Weijun Fang, Anjie Liu","doi":"10.1007/s12013-024-01658-2","DOIUrl":"10.1007/s12013-024-01658-2","url":null,"abstract":"Acute kidney injury (AKI) and acute lung injury (ALI) are major complications of intra-abdominal sepsis, leading to increased mortality. Phellodendrine (PHE) is a characteristic and important active ingredient of Phellodendri Cortex, possessing multiple pharmacological properties. This study intends to explore the effect of PHE on intra-abdominal sepsis-induced AKI and ALI. An intra-abdominal infection-induced rat model of sepsis was established by fecal intraperitoneal injection, followed by the administration of PHE. ELISA was used to determine plasma levels of inflammatory cytokines. Hematoxylin-eosin, Periodic acid Schiff, and Masson trichrome staining were employed for histopathological analysis of rat kidney and lung tissues. Western blotting was used to estimate the AKT/NF-κB signaling-related protein levels. The results showed that PHE improved the survival rate of septic rats and reduced plasma levels of proinflammatory cytokines. PHE administration attenuated pathological lesions in the kidneys and lungs of septic rats. Mechanistically, PHE treatment blocked AKT/NF-κB signaling in septic rats' kidneys and lungs. In conclusion, PHE ameliorates intra-abdominal sepsis-induced kidney and lung injury possibly by inactivating AKT/NF-kB signaling.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"2489-2497"},"PeriodicalIF":1.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143424720","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Salidroside Prevents Keloid Fibroblast Aggressive Progression by Upregulating miR-26a-5p to Inhibit JAG1. 红红草苷通过上调miR-26a-5p抑制JAG1阻止瘢痕疙瘩成纤维细胞侵袭性进展。

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2025-06-01 Epub Date: 2025-01-17 DOI: 10.1007/s12013-025-01667-9

Yanlei Qin, Rongrong Zhang, Weihong Liu, Xunhua Xu, Fangxing Chen

{"title":"Salidroside Prevents Keloid Fibroblast Aggressive Progression by Upregulating miR-26a-5p to Inhibit JAG1.","authors":"Yanlei Qin, Rongrong Zhang, Weihong Liu, Xunhua Xu, Fangxing Chen","doi":"10.1007/s12013-025-01667-9","DOIUrl":"10.1007/s12013-025-01667-9","url":null,"abstract":"Salidroside, a natural herb, exerts considerable anti-tumor effects in various human cancers. Evidence unveils that Salidroside mediates gene expression to affect cancer progression. Our work intended to uncover the molecular mechanism of Salidroside functional role in keloid. Expression analysis for JAG1 and miR-26a-5p in tissues and cells was performed using qRT-PCR or western blotting. For functional analysis, cell proliferation, apoptosis and migration were ascertained by CCK-8, flow cytometry and Transwell assay, respectively. The putative binding relationship between JAG1 and miR-26a-5p was further confirmed by dual-luciferase reporter assay. Salidroside exerted pharmacological properties in keloid and impaired keloid fibroblast (KF) viability. JAG1 was upregulated in keloid tissues, and its expression was repressed by Salidroside in KFs. Salidroside depleted KF proliferation and migration but stimulated apoptosis, and JAG1 knockdown largely strengthened the functional effects of Salidroside. MiR-26a-5p interacted with JAG1 3'UTR and expressed with an opposite pattern with JAG1 in keloid. Inhibition of miR-26a-5p largely abolished the effects of JAG1 knockdown in Salidroside-treated KFs, leading to the recovery of KF aggressive behaviors. Salidroside blocked KF aggressive progression by upregulating miR-26a-5p to inhibit JAG1, which provided evidence on the anti-tumor effects of Salidroside in human keloid.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":" ","pages":"2577-2587"},"PeriodicalIF":1.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142998168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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