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miR-328-5p functions as a critical negative regulator in early endothelial inflammation and advanced atherosclerosis. miR-328-5p 在早期内皮炎症和晚期动脉粥样硬化中发挥关键负调控因子的作用。
IF 2.9 3区 生物学
BMB Reports Pub Date : 2024-08-01
Yangxia Zhang, Yingke Li, Zhisheng Han, Qingyang Huo, Longkai Ji, Xuejia Liu, Han Li, Xinxing Zhu, Zhipeng Hao
{"title":"miR-328-5p functions as a critical negative regulator in early endothelial inflammation and advanced atherosclerosis.","authors":"Yangxia Zhang, Yingke Li, Zhisheng Han, Qingyang Huo, Longkai Ji, Xuejia Liu, Han Li, Xinxing Zhu, Zhipeng Hao","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Early proatherogenic inflammation constitutes a significant risk factor for atherogenesis development. Despite this, the precise molecular mechanisms driving this pathological progression largely remain elusive. Our study unveils a pivotal role for the microRNA miR-328-5p in dampening endothelial inflammation by modulating the stability of JUNB (JunB proto-oncogene). Perturbation of miR-328-5p levels results in heightened monocyte adhesion to endothelial cells and enhanced transendothelial migration, while its overexpression mitigates these inflammatory processes. Furthermore, miR-328-5p hinders macrophage polarization toward the pro-inflammatory M1 phenotype, and exerts a negative influence on atherosclerotic plaque formation in vivo. By pinpointing JUNB as a direct miR-328-5p target, our research underscores the potential of miR-328-5p as a therapeutic target for inflammatory atherosclerosis. Reintroduction of JUNB effectively counteracts the anti-atherosclerotic effects of miR-328-5p, highlighting the promise of pharmacological miR-328-5p targeting in managing inflammatory atherosclerosis. [BMB Reports 2024; 57(8): 375-380].</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"375-380"},"PeriodicalIF":2.9,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11362139/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141449591","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
ASCL1-mediated direct reprogramming: converting ventral midbrain astrocytes into dopaminergic neurons for Parkinson's disease therapy. ASCL1 介导的直接重编程:将腹侧中脑星形胶质细胞转化为治疗帕金森病的多巴胺能神经元。
IF 2.9 3区 生物学
BMB Reports Pub Date : 2024-08-01
Sang Hui Yong, Sang-Mi Kim, Gyeong Woon Kong, Seung Hwan Ko, Eun-Hye Lee, Yohan Oh, Chang-Hwan Park
{"title":"ASCL1-mediated direct reprogramming: converting ventral midbrain astrocytes into dopaminergic neurons for Parkinson's disease therapy.","authors":"Sang Hui Yong, Sang-Mi Kim, Gyeong Woon Kong, Seung Hwan Ko, Eun-Hye Lee, Yohan Oh, Chang-Hwan Park","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Parkinson's disease (PD), characterized by dopaminergic neuron degeneration in the substantia nigra, is caused by various genetic and environmental factors. Current treatment methods are medication and surgery; however, a primary therapy has not yet been proposed. In this study, we aimed to develop a new treatment for PD that induces direct reprogramming of dopaminergic neurons (iDAN). Achaete-scute family bHLH transcription factor 1 (ASCL1) is a primary factor that initiates and regulates central nervous system development and induces neurogenesis. In addition, it interacts with BRN2 and MYT1L, which are crucial transcription factors for the direct conversion of fibroblasts into neurons. Overexpression of ASCL1 along with the transcription factors NURR1 and LMX1A can directly reprogram iDANs. Using a retrovirus, GFP-tagged ASCL1 was overexpressed in astrocytes. One week of culture in iDAN convertsion medium reprogrammed the astrocytes into iDANs. After 7 days of differentiation, TH+/TUJ1+ cells emerged. After 2 weeks, the number of mature TH+/TUJ1+ dopaminergic neurons increased. Only ventral midbrain (VM) astrocytes exhibited these results, not cortical astrocytes. Thus, VM astrocytes can undergo direct iDAN reprogramming with ASCL1 alone, in the absence of transcription factors that stimulate dopaminergic neurons development. [BMB Reports 2024; 57(8): 363-368].</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"363-368"},"PeriodicalIF":2.9,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11362138/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140847983","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
Challenges and innovations in hematopoietic stem cell transplantation: exploring bone marrow niches and new model systems. 造血干细胞移植的挑战与创新:探索骨髓龛位和新模型系统。
IF 2.9 3区 生物学
BMB Reports Pub Date : 2024-08-01
Byung-Chul Lee
{"title":"Challenges and innovations in hematopoietic stem cell transplantation: exploring bone marrow niches and new model systems.","authors":"Byung-Chul Lee","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Hematopoietic stem cell transplantation (HSCT) remains an indispensable therapeutic strategy for various hematological diseases. This review discusses the pivotal role of bone marrow (BM) niches in influencing the efficacy of HSCT and evaluates the current animal models, emphasizing their limitations and the need for alternative models. Traditional animal models, mainly murine xenograft, have provided significant insights, but due to species-specific differences, are often constrained from accurately mimicking human physiological responses. These limitations highlight the importance of developing alternative models that can more realistically replicate human hematopoiesis. Emerging models that include BM organoids and BM-on-a-chip microfluidic systems promise enhanced understanding of HSCT dynamics. These models aim to provide more accurate simulations of the human BM microenvironment, potentially leading to improved preclinical assessments and therapeutic outcomes. This review highlights the complexities of the BM niche, discusses the limitations of current models, and suggests directions for future research using advanced model systems. [BMB Reports 2024; 57(8): 352-362].</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"352-362"},"PeriodicalIF":2.9,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11362137/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141449586","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
Downregulated CDK10 promotes cancer progression and radioresistance in lung cancer through activating the JNK/c-Jun signaling pathway. 下调的 CDK10 通过激活 JNK/c-Jun 信号通路促进肺癌的癌症进展和放射抗性。
IF 2.9 3区 生物学
BMB Reports Pub Date : 2024-07-01
Chaojin Hong, Yimei Meng, Anchen Qiu, Haibo Zhang, Liu Yang, Yupeng Hong, Yumei Huang
{"title":"Downregulated CDK10 promotes cancer progression and radioresistance in lung cancer through activating the JNK/c-Jun signaling pathway.","authors":"Chaojin Hong, Yimei Meng, Anchen Qiu, Haibo Zhang, Liu Yang, Yupeng Hong, Yumei Huang","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Lung cancer is one of the most significant malignancies, with both high morbidity and mortality. CDK10 is closely related to cancer progression and metastasis. However, its role in lung cancer radioresistance demands further clarification. In this study, we demonstrated that CDK10 was downregulated in lung cancer tissues, and CDK10 expression level was associated with the clinical prognosis in lung cancer patients. We also found that silencing CDK10 promoted lung cancer cell proliferation, migration, and radioresistance. We further verified that silencing CDK10 facilitated the activation of JNK/c-Jun signaling, and c-Jun depletion could reverse the effects of CDK10 knockdown in lung cancer cells. Our findings revealed that CDK10 plays an important role in cell growth and radioresistance by inhibiting JNK/c-Jun signaling pathway in lung cancer. Therefore, CDK10 might be a promising therapeutic target in lung cancer. [BMB Reports 2024; 57(7): 336-341].</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"336-341"},"PeriodicalIF":2.9,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11289505/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141449587","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
Prmt7 is required for the osteogenic differentiation of mesenchymal stem cells via modulation of BMP signaling. Prmt7是间充质干细胞通过调节BMP信号分化成骨所必需的。
IF 2.9 3区 生物学
BMB Reports Pub Date : 2024-07-01
Tuan Anh Vuong, Yan Zhang, June Kim, Young-Eun Leem, Jong-Sun Kang
{"title":"Prmt7 is required for the osteogenic differentiation of mesenchymal stem cells via modulation of BMP signaling.","authors":"Tuan Anh Vuong, Yan Zhang, June Kim, Young-Eun Leem, Jong-Sun Kang","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Arginine methylation, which is catalyzed by protein arginine methyltransferases (Prmts), is known to play a key role in various biological processes. However, the function of Prmts in osteogenic differentiation of mesenchymal stem cells (MSCs) has not been clearly understood. In the current study, we attempted to elucidate a positive role of Prmt7 in osteogenic differentiation. Prmt7-depleted C3H/10T1/2 cells or bone marrow mesenchymal stem cells (BMSCs) showed the attenuated expression of osteogenic specific genes and Alizarin red staining compared to the wild-type cells. Furthermore, we found that Prmt7 deficiency reduced the activation of bone morphogenetic protein (BMP) signaling cascade, which is essential for the regulation of cell fate commitment and osteogenesis. Taken together, our data indicate that Prmt7 plays important regulatory roles in osteogenic differentiation. [BMB Reports 2024; 57(7): 330-335].</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"330-335"},"PeriodicalIF":2.9,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11289507/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140858162","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
Identification and structure of AIMP2-DX2 for therapeutic perspectives. 鉴定 AIMP2-DX2 并确定其结构,展望治疗前景。
IF 2.9 3区 生物学
BMB Reports Pub Date : 2024-07-01
Hyeon Jin Kim, Mi Suk Jeong, Se Bok Jang
{"title":"Identification and structure of AIMP2-DX2 for therapeutic perspectives.","authors":"Hyeon Jin Kim, Mi Suk Jeong, Se Bok Jang","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Regulation of cell fate and lung cell differentiation is associated with Aminoacyl-tRNA synthetases (ARS)-interacting multifunctional protein 2 (AIMP2), which acts as a non-enzymatic component required for the multi-tRNA synthetase complex. In response to DNA damage, a component of AIMP2 separates from the multi-tRNA synthetase complex, binds to p53, and prevents its degradation by MDM2, inducing apoptosis. Additionally, AIMP2 reduces proliferation in TGF-β and Wnt pathways, while enhancing apoptotic signaling induced by tumor necrosis factor-β. Given the crucial role of these pathways in tumorigenesis, AIMP2 is expected to function as a broad-spectrum tumor suppressor. The full-length AIMP2 transcript consists of four exons, with a small section of the pre-mRNA undergoing alternative splicing to produce a variant (AIMP2-DX2) lacking the second exon. AIMP2-DX2 binds to FBP, TRAF2, and p53 similarly to AIMP2, but competes with AIMP2 for binding to these target proteins, thereby impairing its tumor-suppressive activity. AIMP2-DX2 is specifically expressed in a diverse range of cancer cells, including breast cancer, liver cancer, bone cancer, and stomach cancer. There is growing interest in AIMP2-DX2 as a promising biomarker for prognosis and diagnosis, with AIMP2-DX2 inhibition attracting significant interest as a potentially effective therapeutic approach for the treatment of lung, ovarian, prostate, and nasopharyngeal cancers. [BMB Reports 2024; 57(7): 318-323].</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"318-323"},"PeriodicalIF":2.9,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11289502/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141247413","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
VSTM2L is a promising therapeutic target and a prognostic soluble-biomarker in cholangiocarcinoma. VSTM2L 是胆管癌中一个很有前景的治疗靶点和预后可溶性生物标志物。
IF 2.9 3区 生物学
BMB Reports Pub Date : 2024-07-01
Jungwhoi Lee, Woogwang Sim, Jungsul Lee, Jae-Hoon Kim
{"title":"VSTM2L is a promising therapeutic target and a prognostic soluble-biomarker in cholangiocarcinoma.","authors":"Jungwhoi Lee, Woogwang Sim, Jungsul Lee, Jae-Hoon Kim","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The aim of the present study is to provide a rational background for silencing the V-set and transmembrane domain containing 2 like (VSTM2L) in consort with recognising soluble VSTM2L against cholangiocarcinoma. A therapeutic target against cholangiocarcinoma was selected using iterative patient partitioning (IPP) calculation, and it was verified by in vitro and in silico analyses. VSTM2L was selected as a potential therapeutic target against cholangiocarcinoma. Silencing the VSTM2L expression significantly attenuated the viability and survival of cholangiocarcinoma cells through blockade of the intracellular signalling pathway. In silico analysis showed that VSTM2L affected the positive regulation of cell growth in cholangiocarcinoma. Liptak's z value revealed that the expression of VSTM2L worsened the prognosis of cholangiocarcinoma patients. In addition, soluble VSTM2L was significantly detected in the whole blood of cholangiocarcinoma patients compared with that of healthy donors. Our report reveals that VSTM2L might be the potential therapeutic target and a soluble prognostic biomarker against cholangiocarcinoma. [BMB Reports 2024; 57(7): 324-329].</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"324-329"},"PeriodicalIF":2.9,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11289506/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140848765","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
Erratum to: Stomach clusterin as a gut-derived feeding regulator. 勘误:作为肠源性摄食调节因子的胃集束素
IF 2.9 3区 生物学
BMB Reports Pub Date : 2024-07-01
Cherl NamKoong, Bohye Kim, Ji Hee Yu, Byung Soo Youn, Hanbin Kim, Evonne Kim, So Young Gil, Gil Myoung Kang, Chan Hee Lee, Young-Bum Kim, Kyeong-Han Park, Min-Seon Kim, Obin Kwon
{"title":"Erratum to: Stomach clusterin as a gut-derived feeding regulator.","authors":"Cherl NamKoong, Bohye Kim, Ji Hee Yu, Byung Soo Youn, Hanbin Kim, Evonne Kim, So Young Gil, Gil Myoung Kang, Chan Hee Lee, Young-Bum Kim, Kyeong-Han Park, Min-Seon Kim, Obin Kwon","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>[Erratum to: BMB Reports 2024; 57(3): 149-154, PMID: 37817436, PMCID: PMC10979347] The BMB Reports would like to correct in BMB Rep. 57(3):149-154, titled \"Stomach clusterin as a gut-derived feeding regulator\". This research was supported by the Creative-Pioneering Researchers Program through Seoul National University. Since grant name and number are incorrect, this information has now been corrected as follows: This work was supported by the National Research Foundation of Korea funded by the Korean government (2020R1A2C3004843, 2022M3E5E8017213 to M-S.K., 2020R1C1C10 08033 to O.K.) and by Creative-Pioneering Researchers Program through Seoul National University (to O.K.). The authors apologize for any inconvenience or confusion that may be caused by this error. The ACKNOWLEDGEMENTS of Original PDF version have been corrected.</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":"57 7","pages":"342"},"PeriodicalIF":2.9,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11289504/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141854674","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
Electrophysiological insights with brain organoid models: a brief review. 脑器官模型的电生理学见解:简要回顾。
IF 2.9 3区 生物学
BMB Reports Pub Date : 2024-07-01
Rian Kang, Soomin Park, Saewoon Shin, Gyusoo Bak, Jong-Chan Park
{"title":"Electrophysiological insights with brain organoid models: a brief review.","authors":"Rian Kang, Soomin Park, Saewoon Shin, Gyusoo Bak, Jong-Chan Park","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Brain organoid is a three-dimensional (3D) tissue derived from stem cells such as induced pluripotent stem cells (iPSCs) embryonic stem cells (ESCs) that reflect real human brain structure. It replicates the complexity and development of the human brain, enabling studies of the human brain in vitro. With emerging technologies, its application is various, including disease modeling and drug screening. A variety of experimental methods have been used to study structural and molecular characteristics of brain organoids. However, electrophysiological analysis is necessary to understand their functional characteristics and complexity. Although electrophysiological approaches have rapidly advanced for monolayered cells, there are some limitations in studying electrophysiological and neural network characteristics due to the lack of 3D characteristics. Herein, electrophysiological measurement and analytical methods related to neural complexity and 3D characteristics of brain organoids are reviewed. Overall, electrophysiological understanding of brain organoids allows us to overcome limitations of monolayer in vitro cell culture models, providing deep insights into the neural network complex of the real human brain and new ways of disease modeling. [BMB Reports 2024; 57(7): 311-317].</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"311-317"},"PeriodicalIF":2.9,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11289503/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141449588","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
T-plastin contributes to epithelial-mesenchymal transition in human lung cancer cells through FAK/AKT/Slug axis signaling pathway. T-plastin 通过 FAK/AKT/Slug 轴信号通路促进人肺癌细胞的上皮-间质转化。
IF 2.9 3区 生物学
BMB Reports Pub Date : 2024-06-01
Soon Yong Park, Hyeongrok Choi, Soo Min Choi, Seungwon Wang, Sangin Shim, Woojin Jun, Jungkwan Lee, Jin Woong Chung
{"title":"T-plastin contributes to epithelial-mesenchymal transition in human lung cancer cells through FAK/AKT/Slug axis signaling pathway.","authors":"Soon Yong Park, Hyeongrok Choi, Soo Min Choi, Seungwon Wang, Sangin Shim, Woojin Jun, Jungkwan Lee, Jin Woong Chung","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>T-plastin (PLST), a member of the actin-bundling protein family, plays crucial roles in cytoskeletal structure, regulation, and motility. Studies have shown that the plastin family is associated with the malignant characteristics of cancer, such as circulating tumor cells and metastasis, by inducing epithelialmesenchymal transition (EMT) in various cancer cells. However, the role of PLST in the EMT of human lung cancer cells remains unclear. In this study, we observed that PLST overexpression enhanced cell migratory and invasive abilities, whereas its downregulation resulted in their suppression. Moreover, PLST expression levels were associated with the expression patterns of EMT markers, including E-cadherin, vimentin, and Slug. Furthermore, the phosphorylation levels of focal adhesion kinase (FAK) and AKT serine/threonine kinase (AKT) were dependent on PLST expression levels. These findings indicate that PLST induces the migration and invasion of human lung cancer cells by promoting Slug-mediated EMT via the FAK/AKT signaling pathway. [BMB Reports 2024; 57(6): 305-310].</p>","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"305-310"},"PeriodicalIF":2.9,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11214894/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141247422","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
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