DNA and cell biology最新文献

筛选
英文 中文
Inherited Spinocerebellar Ataxia Segregates with Intra-Familial Genetic Heterogeneity in a Consanguineous Pakistani Family: A Report of a Potential Novel Candidate Gene. 在一个巴基斯坦近亲家庭中,遗传性脊髓小脑共济失调伴有家族内遗传异质性:一个潜在新候选基因的报告。
DNA and cell biology Pub Date : 2024-11-07 DOI: 10.1089/dna.2024.0130
Yaqi Zhou, Jun Xu, Muhammad Asif, Na Yin, Arusa Ejaz, Mahboob Qadir, Gamal A Shazly, Tao Yang, Lingchao Ji, Xiaochan Lu, Jiatao Zhong, Su Liu, Lei Liu, Yuanyuan Yang, Weiping Ye, Furhan Iqbal, Xueshuang Mei, Hongyi Hu
{"title":"Inherited Spinocerebellar Ataxia Segregates with Intra-Familial Genetic Heterogeneity in a Consanguineous Pakistani Family: A Report of a Potential Novel Candidate Gene.","authors":"Yaqi Zhou, Jun Xu, Muhammad Asif, Na Yin, Arusa Ejaz, Mahboob Qadir, Gamal A Shazly, Tao Yang, Lingchao Ji, Xiaochan Lu, Jiatao Zhong, Su Liu, Lei Liu, Yuanyuan Yang, Weiping Ye, Furhan Iqbal, Xueshuang Mei, Hongyi Hu","doi":"10.1089/dna.2024.0130","DOIUrl":"10.1089/dna.2024.0130","url":null,"abstract":"<p><p>Hereditary spinocerebellar ataxia (SCA) is a group of genetic neurodegenerative disorders caused by a variety of gene variants. At least 44 types of SCAs have been identified to date, and more than 35 genes and hundreds of variants have been reported that are associated with SCAs. We have investigated a Pakistani consanguineous six-generation family with SCA by using whole-exome sequencing analysis. We identified a reported SCA-associated variant, c.C2687G (p.P896R) in <i>CACNA1A</i>, in only a subgroup of the family, while a c.C262T (p.P88S) variant in <i>ARFIP1</i> serves as a candidate pathogenic variant in the other subgroup as a possible novel cause of SCA. Our study showed that intra-familial heterogeneity may exist in SCA families and presented a candidate new causative gene for SCA.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142590923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The Role of lncRNA FEZF1-AS1 in Colorectal Cancer Progression Via the P53 Signaling Pathway. lncRNA FEZF1-AS1 通过 P53 信号通路在结直肠癌进展中的作用
DNA and cell biology Pub Date : 2024-11-06 DOI: 10.1089/dna.2024.0184
Minglu Ding, Wanyao Wang, Keyuan Huo, Yidan Song, Xiaojie Chen, Zihan Xiang, Peijian Chen, Lantao Liu
{"title":"The Role of lncRNA <i>FEZF1-AS1</i> in Colorectal Cancer Progression Via the <i>P53</i> Signaling Pathway.","authors":"Minglu Ding, Wanyao Wang, Keyuan Huo, Yidan Song, Xiaojie Chen, Zihan Xiang, Peijian Chen, Lantao Liu","doi":"10.1089/dna.2024.0184","DOIUrl":"https://doi.org/10.1089/dna.2024.0184","url":null,"abstract":"<p><p>Long noncoding RNAs (lncRNAs) have emerged as critical regulators in the development of colorectal cancer (CRC). Previous studies indicate that lncRNA <i>FEZF1-AS1</i> is highly expressed in CRC, but its role in modulating CRC via the <i>P53</i> signaling pathway remains unclear. In this study, we found that <i>FEZF1-AS1</i> promotes the growth of the CRC cell line (HCT116) and drives epithelial-mesenchymal transition (EMT) through the <i>P53</i> signaling pathway. Our data showed that <i>FEZF1-AS1</i> expression is significantly upregulated in HCT116, and elevated levels of <i>FEZF1-AS1</i> are associated with poor prognosis in patients with CRC. In addition, the knockdown of <i>FEZF1-AS1</i> markedly inhibited the proliferation of HCT116 by inducing cell cycle arrest. Knockdown of <i>FEZF1-AS1</i> depletion also led to apoptosis in CRC cells by suppressing the <i>P53</i> signaling pathway and EMT, thereby reducing their viability, proliferation, migration, and invasion. In summary, this study confirmed that <i>FEZF1-AS1</i> regulates the growth of junction HCT116 through <i>P53</i> signaling pathway and inhibiting EMT, providing new insights for the potential therapeutic strategies against CRC.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142585297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Association Study of rs1632947, rs1233334, and rs371194629 Polymorphisms in Human Leukocyte Antigen G Gene Expression and soluble Human Leukocyte Antigen G with Lupus. 人类白细胞抗原 G 基因表达和可溶性人类白细胞抗原 G 中 rs1632947、rs1233334 和 rs371194629 多态性与红斑狼疮的关联研究
DNA and cell biology Pub Date : 2024-11-06 DOI: 10.1089/dna.2024.0144
Kamil Mahdi Halboot Aljumaili, Mehdi Haghi, Mohammad Khalaj Kondori, Mohammad Reza Ardalan, Mohammad Ali Hosseinpour Feizi
{"title":"Association Study of rs1632947, rs1233334, and rs371194629 Polymorphisms in Human Leukocyte Antigen G Gene Expression and soluble Human Leukocyte Antigen G with Lupus.","authors":"Kamil Mahdi Halboot Aljumaili, Mehdi Haghi, Mohammad Khalaj Kondori, Mohammad Reza Ardalan, Mohammad Ali Hosseinpour Feizi","doi":"10.1089/dna.2024.0144","DOIUrl":"https://doi.org/10.1089/dna.2024.0144","url":null,"abstract":"<p><p>Systemic lupus erythematosus is a chronic autoimmune disease that has been associated with human leukocyte antigen G (HLA-G) in previous studies on immunological diseases. This study aimed to investigate the association between three HLA-G gene polymorphisms (rs1632947, rs1233334, and rs371194629) and their impact on HLA-G mRNA expression and soluble HLA-G levels in serum. Genotyping was performed using TaqMan probe PCR. RNA extraction, reverse transcription PCR, and real-time PCR assays were conducted to assess the expression of the HLA-G gene in tissue samples. Soluble HLA-G was measured using enzyme-linked immunosorbent assay in serum. Results show a significant difference in the frequency of the G allele for two 5'-untranslated region (UTR) polymorphisms of the HLA-G gene (rs1632947 and rs1233334) located at positions -964 and -725, respectively, between lupus patients and controls, with <i>p</i>-values of 0.009 and 0.040, respectively. In addition, the study identified the 14 bp insertion allele of the rs371194629 polymorphism located in the 3' UTR of the gene as a risk factor for lupus, with a <i>p</i>-value of 0.001. Our results also indicate that lupus-related alleles may increase the risk of developing the disease by upregulating the expression of HLA-G and increasing soluble HLA-G levels in serum. The findings of the study suggest that the identified genetic variants may play a role in the development of lupus and could be useful in identifying individuals at risk for the disease. These results are important for advancing our understanding of the genetic basis of lupus and may have implications for the development of new treatments and diagnostic tools for the disease.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142585295","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Histone Lactylation-Driven GPD2 Mediates M2 Macrophage Polarization to Promote Malignant Transformation of Cervical Cancer Progression. 组蛋白乳化驱动的 GPD2 介导 M2 巨噬细胞极化,促进宫颈癌进展的恶性转化。
DNA and cell biology Pub Date : 2024-11-06 DOI: 10.1089/dna.2024.0122
Chenlingzi Huang, Lujiadai Xue, Xinzi Lin, Yuan Shen, Xiaoyu Wang
{"title":"Histone Lactylation-Driven GPD2 Mediates M2 Macrophage Polarization to Promote Malignant Transformation of Cervical Cancer Progression.","authors":"Chenlingzi Huang, Lujiadai Xue, Xinzi Lin, Yuan Shen, Xiaoyu Wang","doi":"10.1089/dna.2024.0122","DOIUrl":"10.1089/dna.2024.0122","url":null,"abstract":"<p><p>Cervical cancer (CC) is the most common cancer in women. This study aims to explore the molecular mechanism of lactate secreted by CC cells modulating macrophage polarization in CC via histone lactylation. Normal cervical epithelium (NCE), low-grade squamous intraepithelial lesion (LSIL), high-grade squamous intraepithelial lesion (HSIL), and cervical squamous cell carcinoma (CESC) were collected to assess H3K18la level and macrophage infiltration. Macrophages were incubated with SiHa cell-derived conditioned medium to detect M1 and M2 markers. NCE, HSIL, and CESC samples were used for ChIP-seq of H3K18la. Histone lactylation-dirven <i>GPD2</i> was knocked down in macrophages. Compared to NCE, H3K18la level and M2 macrophage abundance were increased in LSIL, HSIL, and CESC. Lactate secreted by CC cells upregulated H3K18la and M2 markers but downregulated M1 markers in macrophages. ChIP-seq revealed that upregulated pathways in HSIL vs. NCE and CESC vs. HSIL were commonly enriched in lipid metabolism. Notably, lactate upregulated H3K18la-modified <i>GPD2</i> expression in macrophages, and <i>GPD2</i> knockdown reversed lactate induction to M2 macrophages. Collectively, lactate secreted by CC cells upregulates <i>GPD2</i> via histone lactylation, thereby promoting M2 macrophage polarization in CC. This study provides new insights into the role of histone lactylation in macrophage polarization in the malignant transformation of CC.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142585296","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A Long-Term Follow-Up Study of Serum NFATc3 Levels in Pediatric Patients with Bronchial Asthma: A Prospective Observational Case-Control Investigation. 小儿支气管哮喘患者血清 NFATc3 水平的长期随访研究:一项前瞻性观察病例对照调查
DNA and cell biology Pub Date : 2024-11-06 DOI: 10.1089/dna.2024.0146
Xi Zhang, Xiaojun Duan, Yuan Chen, Lili Wang, Yanping Chen
{"title":"A Long-Term Follow-Up Study of Serum NFATc3 Levels in Pediatric Patients with Bronchial Asthma: A Prospective Observational Case-Control Investigation.","authors":"Xi Zhang, Xiaojun Duan, Yuan Chen, Lili Wang, Yanping Chen","doi":"10.1089/dna.2024.0146","DOIUrl":"https://doi.org/10.1089/dna.2024.0146","url":null,"abstract":"<p><p>The early and precise diagnosis of asthma significantly impacts the long-term health outcomes of pediatric patients. The sensitivity and specificity of current biomarkers, however, are frequently limited. Our study aimed to evaluate the clinical significance of nuclear factor of activated T cells, cytoplasmic 3 (NFATc3), in pediatric bronchial asthma, focusing on its diagnostic and prognostic value for disease severity and recurrence. This observational, prospective case-control study involved 200 pediatric patients with bronchial asthma and 200 age- and sex-matched healthy controls, from January 2020 to January 2023. Follow-up varied from 1 to 3 years. We measured levels of NFATc3 and inflammatory cytokines interleukin-1β (IL-1β), IL-6, and TNF-α via enzyme-linked immunosorbent assay. NFATc3 and IL-1β levels at enrollment were markedly higher in patients with acute exacerbations and those classified as severe, compared with their less severe counterparts. Throughout the study, NFATc3, IL-1β, and IL-6 levels significantly increased in severe or acutely exacerbating cases. The diagnostic value of NFATc3 was assessed through receiver operating characteristic curve analysis, which showed its potential in diagnosing bronchial asthma and identifying severe cases. Spearman's analysis confirmed positive associations between peak NFATc3 and cytokine levels. Importantly, disease type, NFATc3 values at enrollment, as well as peak IL-6 levels were identified as independent risk factors for severe bronchial asthma. Elevated NFATc3 is linked with the severity of pediatric bronchial asthma and serves as a potential biomarker for diagnosis and severity prediction, emphasizing its role in guiding treatment strategies.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142590921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
SNORA71A Downregulation Enhances Gemcitabine Sensitivity in Gallbladder Cancer Cells by Inducing Ferroptosis Through Inhibiting the AKT/NRF2/GPX4 Pathway. SNORA71A 下调可通过抑制 AKT/NRF2/GPX4 通路诱导铁凋亡,从而增强胆囊癌细胞对吉西他滨的敏感性
DNA and cell biology Pub Date : 2024-11-01 Epub Date: 2024-10-15 DOI: 10.1089/dna.2024.0107
Yiyu Qin, Yang Zhou, Hongyan Wu, Haiming Lei, Tingyu Ding, Xinya Shen, Jian Li
{"title":"SNORA71A Downregulation Enhances Gemcitabine Sensitivity in Gallbladder Cancer Cells by Inducing Ferroptosis Through Inhibiting the AKT/NRF2/GPX4 Pathway.","authors":"Yiyu Qin, Yang Zhou, Hongyan Wu, Haiming Lei, Tingyu Ding, Xinya Shen, Jian Li","doi":"10.1089/dna.2024.0107","DOIUrl":"10.1089/dna.2024.0107","url":null,"abstract":"<p><p>Previous findings have indicated a marked upregulation of SNORA71A in gallbladder cancer (GBC) tissues compared to normal samples. However, the precise role and molecular mechanisms of SNORA71A in GBC remain largely unknown. Moreover, gemcitabine (GEM) drug resistance has been found to lead to unfavorable outcomes and recurrence in GBC patients. Therefore, this study aims to investigate the impact of SNORA71A on GBC and explore its potential effects on the sensitivity of GBC cells to GEM. RT-qPCR was conducted to assess SNORA71A level in matched normal and GBC tissues. Cell proliferation was examined through CCK-8 and 5-ethynyl-2'-deoxyuridine (EdU) assays. Additionally, the expression of proteins in GBC cells was analyzed using western blot assay. The level of SNORA71A was notably higher in GBC tissues relative to normal tissues. SNORA71A overexpression led to increased GBC cell proliferation and invasion. Conversely, SNORA71A deficiency strongly suppressed GBC cell proliferation and invasion and triggered cell apoptosis and ferroptosis. Additionally, downregulation of SNORA71A obviously enhanced the antiproliferative and anti-invasive effects of GEM on GBC cells, whereas these changes were reversed by inhibiting ferroptosis. Furthermore, deficiency of SNORA71A further augmented the GEM-induced downregulation of p-Akt, Nrf2, and GPX4 in NOZ cells; however, these effects were reversed by ferroptosis inhibition. Collectively, these findings suggested that downregulation of SNORA71A may increase the sensitivity of GBC cells to GEM by triggering ferroptosis through inhibiting the AKT/NRF2/GPX4 signaling pathway.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"559-569"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142483945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Radiation-Induced Intestinal Injury: Molecular Mechanisms and Therapeutic Status. 辐射诱发的肠道损伤:分子机制和治疗现状。
DNA and cell biology Pub Date : 2024-11-01 Epub Date: 2024-09-05 DOI: 10.1089/dna.2024.0105
Dandan Gao, Heng Zhang, Wanjun Sun, Huaqing Wang, Hui Wang
{"title":"Radiation-Induced Intestinal Injury: Molecular Mechanisms and Therapeutic Status.","authors":"Dandan Gao, Heng Zhang, Wanjun Sun, Huaqing Wang, Hui Wang","doi":"10.1089/dna.2024.0105","DOIUrl":"10.1089/dna.2024.0105","url":null,"abstract":"<p><p>Radiation-induced intestinal injury is one of the most common intestinal complications caused by pelvic and abdominal tumor radiotherapy, severely impacting patients' quality of life. Ionizing radiation, while killing tumor cells, inevitably damages healthy tissue. Radiation-induced enteropathy results from radiation therapy-induced intestinal tissue damage and inflammatory responses. This damage involves various complex molecular mechanisms, including cell apoptosis, oxidative stress, release of inflammatory mediators, disruption of immune responses, and imbalance of intestinal microbiota. A thorough understanding of these molecular mechanisms is crucial for developing effective prevention and treatment strategies.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"537-548"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142134834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The p53/miRNA Axis in Breast Cancer. 乳腺癌中的 p53/miRNA 轴。
DNA and cell biology Pub Date : 2024-11-01 Epub Date: 2024-10-18 DOI: 10.1089/dna.2024.0181
Reza Shah Hosseini, Seyed Mohammad Nouri, Pooja Bansal, Ahmed Hjazi, Harpreet Kaur, Anaheed Hussein Kareem, Abhinav Kumar, Rafil Adnan Hussein Al Zuhairi, Nadhim Allawi Al-Shaheri, Parya Mahdavi
{"title":"The p53/miRNA Axis in Breast Cancer.","authors":"Reza Shah Hosseini, Seyed Mohammad Nouri, Pooja Bansal, Ahmed Hjazi, Harpreet Kaur, Anaheed Hussein Kareem, Abhinav Kumar, Rafil Adnan Hussein Al Zuhairi, Nadhim Allawi Al-Shaheri, Parya Mahdavi","doi":"10.1089/dna.2024.0181","DOIUrl":"10.1089/dna.2024.0181","url":null,"abstract":"<p><p>One of the main health issues in the modern world is cancer, with breast cancer (BC) as one of the most common types of malignancies. Different environmental and genetic risk factors are involved in the development of BC. One of the primary genes implicated in cancer development is the p53 gene, which is also known as the \"gatekeeper\" gene. p53 is involved in cancer development by interacting with numerous pathways and signaling factors, including microRNAs (miRNAs). miRNAs are small noncoding RNA molecules that regulate gene expression by binding to the 3' untranslated region of target mRNAs, resulting in their translational inhibition or degradation. If the p53 gene is mutated or degraded, it can contribute to the risk of BC by disrupting the expression of miRNAs. Similarly, the disruption of miRNAs causes the negative regulation of p53. Therefore, the p53/miRNA axis is a crucial pathway in the progression or prevention of BC, and understanding the regulation and function of this pathway may contribute to the development of new therapeutic strategies to help treat BC.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"549-558"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142483946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Magnesium Lithospermate B Inhibits Colorectal Cancer Cell Progression Through JAK2-STAT3 Signaling. 过磷酸钙 B 镁通过 JAK2-STAT3 信号转导抑制结直肠癌细胞进展
DNA and cell biology Pub Date : 2024-10-29 DOI: 10.1089/dna.2024.0071
Dan Huo, Jinpeng Zhang, Tengfei Ma, Yemao Liu, Jianqing Zhang, Bizhen Dong, Yanjun Lu, Anding Wu, Zhaoxia Jin, Yuping Li
{"title":"Magnesium Lithospermate B Inhibits Colorectal Cancer Cell Progression Through JAK2-STAT3 Signaling.","authors":"Dan Huo, Jinpeng Zhang, Tengfei Ma, Yemao Liu, Jianqing Zhang, Bizhen Dong, Yanjun Lu, Anding Wu, Zhaoxia Jin, Yuping Li","doi":"10.1089/dna.2024.0071","DOIUrl":"10.1089/dna.2024.0071","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is the third most commonly diagnosed cancer and the second leading cause of cancer death worldwide. The discovery of new effective therapeutic drugs is always a priority. Magnesium lithospermate B (MLB), a native polyphenol acid, is the major component of the aqueous extracts from Danshen, a traditional Chinese medicine derived from the dry root and rhizome of <i>Salvia miltiorrhiza</i>. MLB has been reported to have antioxidant, anti-inflammatory, and ion channel-regulating activities in several diseases, including cardiovascular, renal, and neuronal diseases. However, the effect of MLB on cancer progression has not been reported. In this study, a series of cellular and molecular experiments were conducted on two CRC cell lines (HCT116 and SW480) to investigate the effects of. The results demonstrated that MLB exerted inhibitory effects on cell proliferation, migration, and invasion. The administration of 50 mg/kg MLB inhibited tumor growth in HCT116 cells in xenografted models. Importantly, we found that MLB treatment inhibited the Janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 (STAT3) signaling pathway, and activation of JAK2-STAT3 signaling with interleukin 6 or overexpression STAT3 significantly suppressed the inhibitory effect of MLB. These findings provide evidence that MLB could inhibit CRC cell progression <i>in vitro</i> and might serve as a potential therapeutic drug for the treatment of CRC.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142523909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Etomidate Inhibits Hepatic Ischemia-Reperfusion Injury Depending on the Activation of Nrf2-HO-1 Signaling Pathway. 依托咪酯抑制肝缺血再灌注损伤取决于激活 Nrf2-HO-1 信号通路
DNA and cell biology Pub Date : 2024-10-29 DOI: 10.1089/dna.2024.0125
Huajing Shan, Zhifang Wang, Yun Chen, Teng-Fei Ma, Jianqing Zhang, Jinpeng Zhang, Zhonghua Cheng, Liping Jia
{"title":"Etomidate Inhibits Hepatic Ischemia-Reperfusion Injury Depending on the Activation of Nrf2-HO-1 Signaling Pathway.","authors":"Huajing Shan, Zhifang Wang, Yun Chen, Teng-Fei Ma, Jianqing Zhang, Jinpeng Zhang, Zhonghua Cheng, Liping Jia","doi":"10.1089/dna.2024.0125","DOIUrl":"https://doi.org/10.1089/dna.2024.0125","url":null,"abstract":"<p><p>Hepatic ischemia-reperfusion (I/R) injury (HIRI) is recognized as a local aseptic inflammatory response driven by innate immunity and is considered a leading cause of early organ dysfunction and failure following liver transplantation. Etomidate (Eto), an anesthetic drug known for its ability to inhibit inflammatory response and apoptosis, was the focus of our investigation. In this study, we conducted hepatic I/R surgery <i>in vivo</i> on C57 mice, analyzing liver damage through histopathology. Additionally, primary hepatocytes isolated from mice were cultured and subjected to hypoxia/reoxygenation (H/R) insult <i>in vitro</i>, with cell activity assessed using the CCK8 assay and immunofluorescence staining employed to analyze liver inflammatory cell infiltration and apoptosis. Results showed that Eto effectively inhibited liver injury, inflammatory response, and apoptosis induced by HIRI surgery, with the greatest effect observed at an Eto concentration of 10 mg/kg. Furthermore, Eto also showed the ability to inhibit H/R-induced cell damage, inflammatory activation, and apoptosis in primary hepatocytes. Further mechanistic studies revealed that Eto could promote the activation of the Nrf2-HO-1 signaling pathway, and the protective effect of Eto on HIRI was nullified when the Nrf2 inhibitor ML385 was utilized. This study highlights the potential of Eto to protect against HIRI by promoting the Nrf2-HO-1 signaling axis.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142523908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信