Cell Division最新文献_第3页

Mitotic kinases are emerging therapeutic targets against metastatic breast cancer. 有丝分裂激酶是治疗转移性乳腺癌的新兴靶点。

IF 2.3 4区生物学

Cell Division Pub Date : 2024-06-17 DOI: 10.1186/s13008-024-00125-x

Alexandra N Aquino-Acevedo, Joel A Orengo-Orengo, Melanie E Cruz-Robles, Harold I Saavedra

{"title":"Mitotic kinases are emerging therapeutic targets against metastatic breast cancer.","authors":"Alexandra N Aquino-Acevedo, Joel A Orengo-Orengo, Melanie E Cruz-Robles, Harold I Saavedra","doi":"10.1186/s13008-024-00125-x","DOIUrl":"10.1186/s13008-024-00125-x","url":null,"abstract":"This review aims to outline mitotic kinase inhibitors' roles as potential therapeutic targets and assess their suitability as a stand-alone clinical therapy or in combination with standard treatments for advanced-stage solid tumors, including triple-negative breast cancer (TNBC). Breast cancer poses a significant global health risk, with TNBC standing out as the most aggressive subtype. Comprehending the role of mitosis is crucial for understanding how TNBC advances from a solid tumor to metastasis. Chemotherapy is the primary treatment used to treat TNBC. Some types of chemotherapeutic agents target cells in mitosis, thus highlighting the need to comprehend the molecular mechanisms governing mitosis in cancer. This understanding is essential for devising targeted therapies to disrupt these mitotic processes, prevent or treat metastasis, and improve patient outcomes. Mitotic kinases like Aurora kinase A, Aurora Kinase B, never in mitosis gene A-related kinase 2, Threonine-Tyrosine kinase, and Polo-kinase 1 significantly impact cell cycle progression by contributing to chromosome separation and centrosome homeostasis. When these kinases go awry, they can trigger chromosome instability, increase cell proliferation, and activate different molecular pathways that culminate in a transition from epithelial to mesenchymal cells. Ongoing clinical trials investigate various mitotic kinase inhibitors as potential biological treatments against advanced solid tumors. While clinical trials against mitotic kinases have shown some promise in the clinic, more investigation is necessary, since they induce severe adverse effects, particularly affecting the hematopoietic system.","PeriodicalId":49263,"journal":{"name":"Cell Division","volume":"19 1","pages":"21"},"PeriodicalIF":2.3,"publicationDate":"2024-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11184769/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141421528","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

Advances in SIRT3 involvement in regulating autophagy-related mechanisms. SIRT3 参与调节自噬相关机制的研究进展。

IF 2.3 4区生物学

Cell Division Pub Date : 2024-06-12 DOI: 10.1186/s13008-024-00124-y

Shuangyun Xi, Weijun Chen, Yong Ke

{"title":"Advances in SIRT3 involvement in regulating autophagy-related mechanisms.","authors":"Shuangyun Xi, Weijun Chen, Yong Ke","doi":"10.1186/s13008-024-00124-y","DOIUrl":"10.1186/s13008-024-00124-y","url":null,"abstract":"The silencing regulatory factor 2-like protein 3 (SIRT3) is a nicotinamide adenine dinucleotide (NAD+) dependent deacetylase located primarily in the mitochondria. This protein plays an important role in oxidative stress, energy metabolism, and autophagy in multicellular organisms. Autophagy (macroautophagy) is primarily a cytoprotective mechanism necessary for intracellular homeostasis and the synthesis, degradation, and recycling of cellular products. Autophagy can influence the progression of several neural, cardiac, hepatic, and renal diseases and can also contribute to the development of fibrosis, diabetes, and many types of cancer. Recent studies have shown that SIRT3 has an important role in regulating autophagy. Therefore in this study, we aimed to perform a literature review to summarize the role of SIRT3 in the regulation of cellular autophagy. The findings of this study could be used to identify new drug targets for SIRT3-related diseases. Methods: A comprehensive literature review of the mechanism involved behind SIRT3 and autophagy-related diseases was performed. Relevant literature published in Pubmed and Web of Science up to July 2023 was identified using the keywords \"silencing regulatory factor 2-like protein 3\", \"SIRT3\" and \"autophagy\".","PeriodicalId":49263,"journal":{"name":"Cell Division","volume":"19 1","pages":"20"},"PeriodicalIF":2.3,"publicationDate":"2024-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11170824/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141312107","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

Extracellular vesicle-delivered hsa_circ_0090081 regulated by EIF4A3 enhances gastric cancer tumorigenesis. 由 EIF4A3 调控的细胞外囊泡递送的 hsa_circ_0090081 可促进胃癌的发生。

IF 2.3 4区生物学

Cell Division Pub Date : 2024-06-11 DOI: 10.1186/s13008-024-00123-z

Yanjie Mou, Kun Lv

{"title":"Extracellular vesicle-delivered hsa_circ_0090081 regulated by EIF4A3 enhances gastric cancer tumorigenesis.","authors":"Yanjie Mou, Kun Lv","doi":"10.1186/s13008-024-00123-z","DOIUrl":"10.1186/s13008-024-00123-z","url":null,"abstract":"Background: Circular RNA (circRNA) and extracellular vesicles (EVs) in tumors are crucial for the malignant phenotype of tumor cells. Nevertheless, the mechanisms and clinical effects of EV-delivered hsa_circ_0090081 in gastric cancer (GC) are unclear. This study aimed to reveal the effect of eukaryotic translation initiation factor 4A3 (EIF4A3)-mediated hsa_circ_0090081 expression and EV-delivered hsa_circ_0090081 on GC progression.Methods: qRT-PCR was conducted to clarify hsa_circ_0090081 and EIF4A3 levels in GC tissues. Transmission electronic microscopy (TEM), nanoparticle tracking analysis (NTA), and Western blotting identified the EVs isolated from GC cells by ultracentrifugation. The roles of hsa_circ_0090081, EIF4A3, and EV-delivered hsa_circ_0090081 in GC cells were analyzed using Transwell, EdU, and CCK-8 assays. The regulatory role between EIF4A3 and hsa_circ_0090081 was investigated using RIP, qRT-PCR, and Pearson's analysis.Results: Our study showed that hsa_circ_0090081 and EIF4A3 were highly expressed in GC, and hsa_circ_0090081 was associated with poor prognosis. Data revealed that hsa_circ_0090081 inhibition restrained GC cell proliferation, invasion, and migration. Additionally, EIF4A3 could bind to the pre-mRNA of PHEX (linear form of hsa_circ_0090081) to enhance hsa_circ_0090081 expression in GC cells. Moreover, EIF4A3 overexpression nullified the malignant phenotypic suppression caused by hsa_circ_0090081 silencing in GC cells. Furthermore, EVs secreted by GC cells delivered hsa_circ_0090081 to facilitate the malignant progression of targeted GC cells.Conclusion: This study showed that hsa_circ_0090081 was enhanced by EIF4A3 to play a promotive role in GC development. The results may help understand the mechanism of EIF4A3 and EV-delivered hsa_circ_0090081 and offer a valuable GC therapeutic target.","PeriodicalId":49263,"journal":{"name":"Cell Division","volume":"19 1","pages":"19"},"PeriodicalIF":2.3,"publicationDate":"2024-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11165812/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141307159","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

PPP2R2A inhibition contributes to preeclampsia by regulating the proliferation, apoptosis, and angiogenesis modulation potential of mesenchymal stem cells. PPP2R2A抑制通过调节间充质干细胞的增殖、凋亡和血管生成调节潜能，对先兆子痫做出贡献。

IF 2.3 4区生物学

Cell Division Pub Date : 2024-05-11 DOI: 10.1186/s13008-024-00118-w

Yan Liu, Fangle Gu, Jun Gao, Yingyan Gu, Zhiyue Li, Dan Lu, Yanxin Zhang

{"title":"PPP2R2A inhibition contributes to preeclampsia by regulating the proliferation, apoptosis, and angiogenesis modulation potential of mesenchymal stem cells.","authors":"Yan Liu, Fangle Gu, Jun Gao, Yingyan Gu, Zhiyue Li, Dan Lu, Yanxin Zhang","doi":"10.1186/s13008-024-00118-w","DOIUrl":"10.1186/s13008-024-00118-w","url":null,"abstract":"Background: The precise mechanisms underlying preeclampsia (PE) pathogenesis remain unclear. Mesenchymal stem cells (MSCs) are involved in the pathology of PE. The aim of our study was to identify the effects of protein phosphatase 2 regulatory subunit B α (PPP2R2A) on MSCs and ascertain its latent role in the progression of PE.Methods: Reverse-transcription quantitative polymerase chain reaction and western blot analyses were performed to determine the expression of PPP2R2A in decidual tissue and decidual (d)MSCs from healthy pregnant women and patients with PE as well as the expression levels of Bax and Bcl-2 in dMSCs. The levels of p-PI3K, PI3K, p-AKT, and AKT were determined using western blotting. Cell growth, apoptosis, and migration were analyzed using MTT, flow cytometry, and Transwell assays, respectively. Human umbilical vein endothelial cell (HUVEC) tube formation ability was assayed using a HUVEC capillary-like tube formation assay.Results: PPP2R2A was downregulated in decidual tissues and dMSCs of patients with PE when compared with that in healthy pregnant women. Moreover, upregulation of PPP2R2A enhanced cell proliferation, reduced apoptotic dMSC, inhibited Bax expression, and increased Bcl-2 levels. Conditioned medium from PPP2R2A-overexpressing dMSCs promoted HTR-8/SVneo cell migration and angiogenesis of HUVEC. Furthermore, the PPP2R2A plasmid suppressed PI3K/AKT pathway activation in dMSCs. However, these effects were partially reversed by LY2940002 treatment.Conclusion: PPP2R2A inhibition contributes to PE by regulating the proliferation, apoptosis, and angiogenesis of MSCs, providing a new therapeutic target for PE diagnosis and treatment.","PeriodicalId":49263,"journal":{"name":"Cell Division","volume":"19 1","pages":"18"},"PeriodicalIF":2.3,"publicationDate":"2024-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11088123/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140908041","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

LncRNA NUTM2A-AS1 silencing inhibits glioma via miR-376a-3p/YAP1 axis. LncRNA NUTM2A-AS1 沉默通过 miR-376a-3p/YAP1 轴抑制胶质瘤。

IF 2.3 4区生物学

Cell Division Pub Date : 2024-05-10 DOI: 10.1186/s13008-024-00122-0

Yuecheng Zeng, Zhenyu Yang, Yang Yang, Peng Wang

{"title":"LncRNA NUTM2A-AS1 silencing inhibits glioma via miR-376a-3p/YAP1 axis.","authors":"Yuecheng Zeng, Zhenyu Yang, Yang Yang, Peng Wang","doi":"10.1186/s13008-024-00122-0","DOIUrl":"10.1186/s13008-024-00122-0","url":null,"abstract":"The lncRNA NUTM2A-AS1 has been shown to be dysregulated in gastric cancer, while the roles in glioma is unclear. The aim of this study was to investigate the roles and potential mechanisms of lncRNA NUTM2A-AS1 in the proliferation and apoptosis of glioma cells. The StarBase software and dual luciferase reporter assay were used to identify the relationship between lncRNA NUTM2A-AS1 and miR-376a-3p, and miR-376a-3p and YAP1. The expression of lncRNA NUTM2A-AS1, miR-376a-3p, and YAP1 in human glioma cell lines was detected by qRT-PCR. MTT and flow cytometry were used to detect the effects of lncRNA NUTM2A-AS1 or miR-376a-3p on the proliferation and apoptosis of U251 and A172 cells, respectively. In addition, changes of Bax and Bcl-2 expression in glioma cells were further verified by western blotting and qRT-PCR. The results showed that the expression of lncRNA NUTM2A-AS1 was elevated in glioma cell lines, while miR-376a-3p was decreased. LncRNA NUTM2A-AS1 was negatively correlated with miR-376a-3p. Silencing of lncRNA NUTM2A-AS1 enhanced the levels of miR-376a-3p, leading to reduced cell proliferation and increased apoptosis in glioma cells. YAP1 was a direct target of miR-376a-3p, and it was negatively regulated by miR-376a-3p in U251 and A172 cells. Further mechanistic studies suggested that miR-376a-3p reduced glioma cell proliferation and increased apoptosis by inhibiting YAP1 expression. In addition, lncRNA NUTM2A-AS1 positively regulated of YAP1 expression in glioma cells. In conclusion, silencing of lncRNA NUTM2A-AS1 inhibited proliferation and induced apoptosis in human glioma cells via the miR-376a-3p/YAP1 axis.","PeriodicalId":49263,"journal":{"name":"Cell Division","volume":"19 1","pages":"17"},"PeriodicalIF":2.3,"publicationDate":"2024-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11088135/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140905128","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

GTSE1 promotes nasopharyngeal carcinoma proliferation and angiogenesis by upregulating STMN1 GTSE1 通过上调 STMN1 促进鼻咽癌的增殖和血管生成

IF 2.3 4区生物学

Cell Division Pub Date : 2024-05-02 DOI: 10.1186/s13008-024-00119-9

Jiadi Dong, Jingjing Chen, Yidong Wu, Jiangyu Yan

{"title":"GTSE1 promotes nasopharyngeal carcinoma proliferation and angiogenesis by upregulating STMN1","authors":"Jiadi Dong, Jingjing Chen, Yidong Wu, Jiangyu Yan","doi":"10.1186/s13008-024-00119-9","DOIUrl":"https://doi.org/10.1186/s13008-024-00119-9","url":null,"abstract":"Nasopharyngeal carcinoma (NPC) is a malignant tumor with poor survival rate. G2 and S phase-expressed‐1 (GTSE1) takes part in the progression of diverse tumors as an oncogene, but its role and potential mechanism in NPC remain unknown. The GTSE1 expression was analyzed by western blot in NPC tissues and cells. Knock-down experiments were conducted to determine the function of GTSE1 in NPC by cell counting kit-8, the 5-ethynyl-2′-deoxyuridine (EdU) incorporation experiment, cell scratch wound-healing experiment, transwell assays, tube forming experiment and western blot. In addition, the in vivo role of GTSE1 was addressed in tumor-bearing mice. The expression of was increased in NPC. Silencing of GTSE1 suppressed cell viability, the percent of EdU positive cells, and the number of invasion cells and tubes, but enhanced the scratch ratio in NPC cells. Mechanically, downregulation of GTSE1 decreased the expressions of FOXM1 and STMN1, which were restored with the upregulation of FOXM1. Increased expression of STMN1 reversed the effects of the GTSE1 silencing on proliferation, migration, invasion and angiogenesis of NPC cells. Furthermore, knockdown of GTSE1 repressed the tumor volume and tumor weight of xenografted mice. GTSE1 was highly expressed in NPC, and silencing of GTSE1 ameliorated the malignant processes of NPC cells by upregulating STMN1, suggesting a possible therapeutical target for NPC.","PeriodicalId":49263,"journal":{"name":"Cell Division","volume":"17 1","pages":""},"PeriodicalIF":2.3,"publicationDate":"2024-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140841168","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

SYVN1 modulates papillary thyroid carcinoma progression by destabilizing HMGB1 SYVN1通过破坏HMGB1的稳定性调节甲状腺乳头状癌的进展

IF 2.3 4区生物学

Cell Division Pub Date : 2024-04-28 DOI: 10.1186/s13008-024-00121-1

Fei Duan, Fanli Kong, Taifeng Jiang, Hongbing Liu

引用次数: 0

Cancer radioresistance is characterized by a differential lipid droplet content along the cell cycle 癌症的放射抗性以细胞周期中不同的脂滴含量为特征

IF 2.3 4区生物学

Cell Division Pub Date : 2024-04-20 DOI: 10.1186/s13008-024-00116-y

Francesca Pagliari, Jeannette Jansen, Jan Knoll, Rachel Hanley, Joao Seco, Luca Tirinato

{"title":"Cancer radioresistance is characterized by a differential lipid droplet content along the cell cycle","authors":"Francesca Pagliari, Jeannette Jansen, Jan Knoll, Rachel Hanley, Joao Seco, Luca Tirinato","doi":"10.1186/s13008-024-00116-y","DOIUrl":"https://doi.org/10.1186/s13008-024-00116-y","url":null,"abstract":"Cancer radiation treatments have seen substantial advancements, yet the biomolecular mechanisms underlying cancer cell radioresistance continue to elude full understanding. The effectiveness of radiation on cancer is hindered by various factors, such as oxygen concentrations within tumors, cells’ ability to repair DNA damage and metabolic changes. Moreover, the initial and radiation-induced cell cycle profiles can significantly influence radiotherapy responses as radiation sensitivity fluctuates across different cell cycle stages. Given this evidence and our prior studies establishing a correlation between cancer radiation resistance and an increased number of cytoplasmic Lipid Droplets (LDs), we investigated if LD accumulation was modulated along the cell cycle and if this correlated with differential radioresistance in lung and bladder cell lines. Our findings identified the S phase as the most radioresistant cell cycle phase being characterized by an increase in LDs. Analysis of the expression of perilipin genes (a family of proteins involved in the LD structure and functions) throughout the cell cycle also uncovered a unique gene cell cycle pattern. In summary, although these results require further molecular studies about the mechanisms of radioresistance, the findings presented here are the first evidence that LD accumulation could participate in cancer cells’ ability to better survive X-Ray radiation when cells are in the S phase. LDs can represent new players in the radioresistance processes associated with cancer metabolism. This could open new therapeutic avenues in which the use of LD-interfering drugs might enhance cancer sensitivity to radiation.","PeriodicalId":49263,"journal":{"name":"Cell Division","volume":"21 1","pages":""},"PeriodicalIF":2.3,"publicationDate":"2024-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140624229","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

Klotho-mediated activation of the anti-oxidant Nrf2/ARE signal pathway affects cell apoptosis, senescence and mobility in hypoxic human trophoblasts: involvement of Klotho in the pathogenesis of preeclampsia Klotho介导的抗氧化Nrf2/ARE信号通路激活影响缺氧人滋养细胞的细胞凋亡、衰老和移动性：Klotho参与子痫前期的发病机制

IF 2.3 4区生物学

Cell Division Pub Date : 2024-04-17 DOI: 10.1186/s13008-024-00120-2

Baomei Xu, Fang Cheng, Xiaolei Xue

{"title":"Klotho-mediated activation of the anti-oxidant Nrf2/ARE signal pathway affects cell apoptosis, senescence and mobility in hypoxic human trophoblasts: involvement of Klotho in the pathogenesis of preeclampsia","authors":"Baomei Xu, Fang Cheng, Xiaolei Xue","doi":"10.1186/s13008-024-00120-2","DOIUrl":"https://doi.org/10.1186/s13008-024-00120-2","url":null,"abstract":"The anti-aging gene Klotho is implicated in the pathogenesis of preeclampsia (PE), which is a pregnancy disease characterized by hypertension and proteinuria. Oxidative stress is closely associated with the worse outcomes in PE, and Klotho can eliminate Reactive Oxygen Species (ROS), but it is still unclear whether Klotho regulates PE pathogenesis through modulating oxidative damages. Here, by analyzing the clinical data, we found that Klotho was aberrantly downregulated in PE umbilical cord serum and placental tissues, compared to their normal counterparts. In in vitro experiments, the human trophoblasts were subjected to hypoxic pressure to establish the PE models, and we confirmed that hypoxia also decreased the expression levels of Klotho in those trophoblasts. In addition, through performing functional experiments, we confirmed that hypoxia promoted oxidative damages, cell apoptosis and senescence, whereas suppressed cell invasion in human trophoblasts, which were all reversed overexpressing Klotho. The following mechanical experiments verified that Klotho increased the levels of nuclear Nrf2, total Nrf2, SOD2 and NQO1 to activate the anti-oxidant Nrf2/ARE signal pathway, and silencing of Nrf2 abrogated the protective effects of Klotho overexpression on hypoxic human trophoblasts. Consistently, in in vivo experiments, Klotho overexpression restrained oxidative damages and facilitated cell mitosis in PE rats’ placental tissues. In conclusion, this study validated that Klotho activated the Nrf2/ARE signal pathway to eliminate hypoxia-induced oxidative damages, cell apoptosis and senescence to recover normal cellular functions in human trophoblasts, and our data supported that Klotho could be used as novel biomarker for PE diagnosis and treatment.","PeriodicalId":49263,"journal":{"name":"Cell Division","volume":"4 1","pages":""},"PeriodicalIF":2.3,"publicationDate":"2024-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140610914","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

lncRNA RMST is associated with the progression and prognosis of gastric cancer via miR-204-5p lncRNA RMST通过miR-204-5p与胃癌的进展和预后有关

IF 2.3 4区生物学

Cell Division Pub Date : 2024-04-12 DOI: 10.1186/s13008-024-00117-x

Huimei Cai, Chenhui Li, Zhou Wu

引用次数: 0