Experimental cell research最新文献_第7页

Chronic hypoxia promotes pulmonary venous smooth muscle cell proliferation through the CaSR-TRPC6/ROCE pathway 慢性缺氧通过CaSR-TRPC6/ROCE通路促进肺静脉平滑肌细胞增殖。

IF 3.3 3区生物学 Q3 CELL BIOLOGY

Experimental cell research

Pub Date : 2025-01-15 DOI: 10.1016/j.yexcr.2024.114363

Shaoxing Li , Zhenli Fu , Wei Hong , Hong Yuan , Weitao Cao , Juan Xu , Rongmin Liu , Zhuandi Lin , Zhiming Xiang , Gongyong Peng

The mechanism underlying chronic hypoxia (CH)-induced pulmonary venous remodeling remains unclear. Cell proliferation is key in vascular remodeling, and the calcium-sensing receptor (CaSR) protein contributes to CH-induced pulmonary venous smooth muscle cell (PVSMC) proliferation. In pulmonary arterial smooth muscle cells, CaSR and transient receptor potential canonical (TRPC) proteins interact, contributing to CH-induced cell proliferation via CaSR-TRPC1/6 signaling. We investigated whether a similar pathway exists in PVSMCs. Rat PVSMCs were isolated and subjected to CH. Cell proliferation was assessed by cell counting, CCK-8, and BrdU incorporation assays. Expression of CaSR and TRPC was analyzed by qPCR and western blotting, while interactions between CaSR and TRPC were detected by co-immunoprecipitation assay. Extracellular Ca²⁺ restoration was evaluated, to assess store- and receptor-operated Ca²⁺ entry (SOCE and ROCE, respectively). CH enhanced PVSMC numbers, viability, and DNA synthesis, and upregulated CaSR and TRPC6 expression. Further, CaSR and TRPC6 interacted with one another. CaSR inhibitors (NPS2143, NPS2390) reduced, whereas activators (spermine, R568) enhanced, CH-induced increases in PVSMC numbers, viability, DNA synthesis, and TRPC6 expression. CaSR knockdown using siRNA inhibited CH-induced TRPC6 upregulation and attenuated CH-induced increases in PVSMC numbers, viability, and DNA synthesis. TRPC6 knockdown had no significant effect on CH-induced CaSR upregulation, but significantly attenuated CH-induced increases in PVSMC number, viability, and DNA synthesis. CaSR knockdown reduced ROCE, but not SOCE, enhancement. Overall, CH promotes PVSMC proliferation through the CaSR-TRPC6/ROCE pathway.

慢性缺氧（CH）诱导肺静脉重构的机制尚不清楚。细胞增殖是血管重构的关键，钙敏感受体（CaSR）蛋白参与ch诱导的肺静脉平滑肌细胞（PVSMC）增殖。在肺动脉平滑肌细胞中，CaSR和瞬时受体电位规范（TRPC）蛋白相互作用，通过CaSR- trpc1 /6信号传导促进ch诱导的细胞增殖。我们研究了PVSMCs中是否存在类似的途径。分离大鼠PVSMCs并进行CH处理。通过细胞计数、CCK-8和BrdU掺入测定来评估细胞增殖。采用qPCR和western blotting分析CaSR和TRPC的表达，采用共免疫沉淀法检测CaSR和TRPC的相互作用。评估细胞外Ca2+恢复，以评估储存和受体操作的Ca2+进入（分别为SOCE和ROCE）。CH增加了PVSMC的数量、活力和DNA合成，上调了CaSR和TRPC6的表达。此外，CaSR和TRPC6相互作用。CaSR抑制剂（NPS2143, NPS2390）减少，而激活剂（精胺，R568）增强，ch诱导PVSMC数量，活力，DNA合成和TRPC6表达增加。使用siRNA敲低CaSR抑制ch诱导的TRPC6上调，并减弱ch诱导的PVSMC数量、活力和DNA合成的增加。TRPC6敲低对ch诱导的CaSR上调无显著影响，但可显著减弱ch诱导的PVSMC数量、活力和DNA合成的增加。CaSR敲除降低了ROCE，但没有提高SOCE。总的来说，CH通过CaSR-TRPC6/ROCE途径促进PVSMC增殖。

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引用次数: 0

Quercetin promotes osteogenic differentiation of bone marrow mesenchymal stem cells by modulating the miR-214-3p/Wnt3a/β-catenin signaling pathway 槲皮素通过调节miR-214-3p/Wnt3a/β-catenin信号通路促进骨髓间充质干细胞成骨分化。

IF 3.3 3区生物学 Q3 CELL BIOLOGY

Experimental cell research

Pub Date : 2025-01-15 DOI: 10.1016/j.yexcr.2024.114386

Xueling Hu , Xiaotong Lei , Weiwen Lin , Xiaoyun Li , Wenqiang Zhong , Bingjie Luo , Ji Xie , Ziwen Liang , Yunchuan Li , Jingli Qiu , Panpan Wang , Xiaofeng Zhu , Ronghua Zhang , Li Yang

Postmenopausal osteoporosis, primarily driven by estrogen deficiency, is predominantly mediated through estrogen receptors such as ERα. However, the underlying mechanisms necessitate further investigation. In this study, we established an ERα-deficient model in rBMSCs to elucidate the role of ERα in osteogenic differentiation and miRNA expression profiles. Our findings demonstrate that knockdown of ERα inhibits osteogenic differentiation in rBMSCs, resulting in upregulation of 25 miRNAs and downregulation of 184 miRNAs, including a significant increase in the expression of miR-214-3p. Validation using qPCR, Western blotting, and bioinformatics analysis revealed that miR-214-3p negatively regulates osteogenic differentiation via the Wnt/β-catenin signaling pathway. Furthermore, we explored the potential therapeutic effects of quercetin (QUE) on rBMSCs. CCK8, alkaline phosphatase activity assays, and Alizarin Red staining demonstrated that QUE dose-dependently enhances rBMSCs proliferation, alkaline phosphatase activity, and mineralization within the concentration range of 0.1–1 μM. Importantly, QUE was found to downregulate miR-214-3p expression and activate the Wnt3a/β-catenin signaling pathway. Rescue experiments confirmed that QUE could counteract the inhibitory effects of miR-214-3p on the Wnt3a/β-catenin signaling pathway. Collectively, our study provides compelling evidence that knockdown of ERα inhibits the osteogenic differentiation of rBMSCs by affecting the miRNA expression profile, while QUE can reverse the inhibitory effect exerted by miR-214-3p on the Wnt3a/β-catenin signaling pathway, thereby offering novel insights into diagnosis, prevention, and treatment strategies for postmenopausal osteoporosis.

绝经后骨质疏松主要由雌激素缺乏引起，主要通过雌激素受体如ERα介导。然而，潜在的机制需要进一步的研究。在本研究中，我们在骨髓间充质干细胞中建立了ERα缺失模型，以阐明ERα在成骨分化和miRNA表达谱中的作用。我们的研究结果表明，ERα的下调抑制了rBMSCs的成骨分化，导致25个mirna的上调和184个mirna的下调，包括miR-214-3p的表达显著增加。qPCR、Western blotting和生物信息学分析验证表明，miR-214-3p通过Wnt/β-catenin信号通路负调控成骨分化。此外，我们还探讨了槲皮素（QUE）对rBMSCs的潜在治疗作用。CCK8、碱性磷酸酶活性测定和茜素红染色表明，QUE在0.1-1 μM浓度范围内呈剂量依赖性地增强rBMSCs的增殖、碱性磷酸酶活性和矿化。重要的是，QUE被发现下调miR-214-3p表达并激活Wnt3a/β-catenin信号通路。救援实验证实，QUE可以抵消miR-214-3p对Wnt3a/β-catenin信号通路的抑制作用。总之，我们的研究提供了令人信服的证据，表明ERα的下调通过影响miRNA的表达谱来抑制rBMSCs的成骨分化，而QUE可以逆转miR-214-3p对Wnt3a/β-catenin信号通路的抑制作用，从而为绝经后骨质疏松症的诊断、预防和治疗策略提供了新的见解。

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引用次数: 0

Combined injection of pristane and Bacillus Calmette-Guerin Vaccine successfully establishes a lupus model with atherosclerosis 普里斯坦与卡介苗联合注射成功建立了伴有动脉粥样硬化的狼疮模型。

IF 3.3 3区生物学 Q3 CELL BIOLOGY

Experimental cell research

Pub Date : 2025-01-15 DOI: 10.1016/j.yexcr.2024.114381

Chunru Jiang , Zhenduo Zhu , Yu Tai , Meiyue Lu , Huijuan Cheng , Tiantian Su , Paipai Guo , Ruhong Fang , Feng He , Mingli Ge , Qiuyun Guan , Yongsheng Han , Shangxue Yan , Wei Wei , Qingtong Wang

Cardiovascular disease (CVD) induced by atherosclerosis (AS) is the main fatal complication of systemic lupus erythematosus (SLE). Establishing an appropriate animal model of SLE with AS is of great value for investigating the pathogenesis and therapeutic targets of SLE-CVD. In the present work, pristane was injected intraperitoneally into C57BL/6J mice to establish the SLE model and Bacillus Calmette-Guerin Vaccine (BCG) was injected intradermally one month later to enhance immunity and induce AS. Both pristane or pristane and BCG treated C57BL/6J mice exhibit a classical lupus-like phenotype which manifested as proteinuria and high levels of serum anti-ANA and anti-dsDNA autoantibodies, in conjunction with pathological changes in spleen and kidney, complement C3 deposition in the kidney, overactivation of T and B cells, a decreased proportion of splenic CD19⁺ B cells, and an increased frequency of CD19⁻CD138⁺ plasma cells, CD19⁺CD27⁺ memory B cells, CD3⁺CD4⁺ helper T (Th) cells, and CD3⁺CD4⁺CXCR5⁺PD-1⁺ T follicular helper cells. The combined pristane and BCG challenge aggravated AS in SLE mice, which had an enlarged thymus gland, an increased T cell proliferative vitality, an expanded Th cell pool, severe perivascular lymphocytes, and CD68⁺ macrophage infiltration, in addition to an intimal lipid deposition, and further elevation of Toll-like receptor 2 (TLR2), TLR4, and the transcription factor nuclear factor-κB (NF-κB) expression in kidney tissue and blood vessels when comparing with pristane or BCG injection alone. Pristane combined BCG challenge is able to establish a validated SLE-AS mouse model in C57BL/6J mice.

动脉粥样硬化（AS）诱发的心血管疾病（CVD）是系统性红斑狼疮（SLE）的主要致命并发症。建立合适的SLE合并AS动物模型，对探讨SLE- cvd的发病机制和治疗靶点具有重要价值。本研究通过C57BL/6J小鼠腹腔注射普里斯坦建立SLE模型，1个月后腹腔注射卡介苗（Bacillus calmetet - guerin Vaccine， BCG）增强免疫，诱导AS。普里斯坦或普里斯坦加卡介苗治疗的C57BL/6J小鼠均表现出典型的狼疮样表型，表现为蛋白尿，血清抗ana和抗dsdna自身抗体水平升高，同时伴有脾和肾的病理改变，补体C3在肾内沉积，T和B细胞过度活化，脾CD19+ B细胞比例降低，CD19- cd138 +浆细胞、CD19+CD27+记忆B细胞、CD3+CD4+辅助性T （Th）细胞频率增加。CD3+CD4+CXCR5+PD-1+ T滤泡辅助细胞。与单独注射普利斯坦或卡介苗相比，普利斯坦和卡介苗联合刺激加重了SLE小鼠的AS，其胸腺增大，T细胞增殖活力增加，Th细胞池扩大，血管周围淋巴细胞严重，CD68+巨噬细胞浸润，内膜脂质沉积，肾组织和血管中toll样受体2 （TLR2）、TLR4和转录因子核因子-κB （NF-κB）表达进一步升高。Pristane联合BCG攻毒能够在C57BL/6J小鼠中建立有效的SLE-AS小鼠模型。

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引用次数: 0

Targeting METTL8 with Rabdosiin overcomes lenvatinib resistance in hepatocellular carcinoma Rabdosiin对mettl8介导的肝细胞癌Lenvatinib耐药的鉴定和靶向治疗

IF 3.3 3区生物学 Q3 CELL BIOLOGY

Experimental cell research

Pub Date : 2025-01-15 DOI: 10.1016/j.yexcr.2024.114389

Yunpeng Liu , Muhua Chen , Xiang-Xu Wang , Yuan Gao , Xiao Han , Shuning Wang , Wangqian Zhang , Xiaoying Lei , Pengfei Yu , Lei Liu , Hong-Mei Zhang , Kuo Zhang

In hepatocellular carcinoma (HCC), lenvatinib is a key first-line treatment that significantly improves survival in some patients with advanced stage. However, lenvatinib resistance presents a major clinical challenge. This study aims to identify key molecular factors driving lenvatinib resistance in HCC and propose intervention strategies to overcome this resistance, thereby enhancing therapeutic efficacy. A genome-wide CRISPR-Cas9 activation screen identified METTL8 as a crucial gene associated with lenvatinib resistance. Validation through in vitro and in vivo assays confirmed METTL8's role in mediating lenvatinib resistance. Higher METTL8 expression was observed in lenvatinib-resistant HCC cells compared to parental cells. Immunohistochemical staining of tissue sections from HCC patients revealed a negative correlation between high METTL8 expression and lenvatinib sensitivity. To inhibit the function of METTL8 that mediate lenvatinib resistance, we conducted a screening using a natural compound library, virtual drug screening identified Rabdosiin as a potential METTL8 inhibitor, subsequent experiments demonstrated that Rabdosiin could effectively overcome METTL8-mediated lenvatinib resistance. In conclusion, this research highlights METTL8 as a novel target for mitigating lenvatinib resistance, proposing that targeting METTL8 could restore lenvatinib sensitivity in HCC, and underscores its value as a biomarker for lenvatinib application in clinical settings.

在肝细胞癌（HCC）中，lenvatinib是一种关键的一线治疗药物，可以显著提高一些晚期患者的生存率。然而，lenvatinib耐药是一个重大的临床挑战。本研究旨在确定HCC中lenvatinib耐药的关键分子因素，并提出克服这种耐药的干预策略，从而提高治疗效果。全基因组CRISPR-Cas9激活筛选发现METTL8是与lenvatinib耐药相关的关键基因。体外和体内实验验证了METTL8介导lenvatinib耐药的作用。与亲代细胞相比，在lenvatinib耐药HCC细胞中观察到更高的METTL8表达。肝癌患者组织切片免疫组化染色显示METTL8高表达与lenvatinib敏感性呈负相关。为了抑制METTL8介导lenvatinib耐药的功能，我们利用天然化合物文库进行筛选，虚拟药物筛选鉴定出Rabdosiin为潜在的METTL8抑制剂，随后的实验证明Rabdosiin可以有效克服METTL8介导的lenvatinib耐药。总之，本研究强调了METTL8作为减轻lenvatinib耐药的新靶点，提出靶向METTL8可以恢复lenvatinib在HCC中的敏感性，并强调了其作为lenvatinib在临床应用的生物标志物的价值。

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引用次数: 0

Mechanism of RBM15 in the malignant proliferation of colorectal cancer cells through regulating the stability of LncRNA FGD5-AS1 via m6A modification RBM15通过m6A修饰调控LncRNA FGD5-AS1的稳定性参与结直肠癌细胞恶性增殖的机制

IF 3.3 3区生物学 Q3 CELL BIOLOGY

Experimental cell research

Pub Date : 2025-01-15 DOI: 10.1016/j.yexcr.2024.114384

Lin Ma , Weihua Liu , Xin Wang , Dezheng Li , Chuankui Wei

Colorectal cancer (CRC) is the third most prevalent cancer all around the world. This study explored the mechanism of RBM15-mediated m6A modification in CRC cell malignant proliferation. The expression of RBM15, LncRNA FGD5-AS1, and HOXC10 was detected in CRC cells. m6A levels in cells and m6A enrichment on FGD5-AS1 RNA were analyzed. FGD5-AS1 RNA stability and localization in CRC cells were analyzed. The binding of LncRNA FGD5-AS1 to YBX1 and YBX1 to the HOXC10 promoter was analyzed. Combined experiments were conducted to validate the mechanism. Tumor xenografts in nude mice were used to verify the mechanism of RBM15 in vivo. RBM15 was highly expressed in CRC cells. RBM15 inhibition suppressed CRC cell proliferation and reduced PCNA expression. RBM15 increased m6A modification on FGD5-AS1 RNA, enhancing FGD5-AS1 stability and expression. FGD5-AS1 promoted HOXC10 expression by recruiting YBX1 to the HOXC10 promoter. YBX1 inhibition suppressed HOXC10 expression. Overexpression of FGD5-AS1 or HOXC10 partially reversed the alleviative effect of RBM15 inhibition on CRC cell proliferation. RBM15 downregulation attenuated in vivo CRC cell proliferation by inhibiting the FGD5-AS1/HOXC10 axis. In conclusion, RBM15 promotes the FGD5-AS1/HOXC10 axis via m6A modification to promote CRC cell proliferation.

结直肠癌（CRC）是世界上第三大常见癌症。本研究探讨了rbm15介导的m6A修饰在结直肠癌细胞恶性增殖中的作用机制。在结直肠癌细胞中检测到RBM15、LncRNA FGD5-AS1和HOXC10的表达。分析细胞内m6A水平及FGD5-AS1 RNA上m6A的富集情况。分析FGD5-AS1 RNA在结直肠癌细胞中的稳定性和定位。分析LncRNA FGD5-AS1与YBX1和YBX1与HOXC10启动子的结合。通过联合实验验证了其机理。采用裸鼠肿瘤异种移植实验验证RBM15在体内的作用机制。RBM15在结直肠癌细胞中高表达。抑制RBM15抑制结直肠癌细胞增殖，降低PCNA表达。RBM15增加了m6A对FGD5-AS1 RNA的修饰，增强了FGD5-AS1的稳定性和表达。FGD5-AS1通过将YBX1募集到HOXC10启动子中来促进HOXC10的表达。抑制YBX1抑制HOXC10的表达。FGD5-AS1或HOXC10的过表达部分逆转了RBM15抑制对结直肠癌细胞增殖的缓解作用。RBM15下调通过抑制FGD5-AS1/HOXC10轴而减弱体内CRC细胞增殖。综上所述，RBM15通过m6A修饰促进FGD5-AS1/HOXC10轴促进CRC细胞增殖。

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引用次数: 0

Paradigm shift: microRNAs interact with target gene promoters to cause transcriptional gene activation or silencing 范式转换：microRNAs与靶基因启动子相互作用，导致转录基因激活或沉默。

IF 3.3 3区生物学 Q3 CELL BIOLOGY

Experimental cell research

Pub Date : 2025-01-15 DOI: 10.1016/j.yexcr.2024.114372

Neelanjana Sarkar, Arun Kumar

MicroRNAs (miRNAs/miRs) are small (18–25 nucleotides in length), endogenous, non-coding RNAs that typically repress gene expression by interacting with the 3′untranslated regions (3′UTRs) of target mRNAs in the cytoplasm. While most of the scientific community still views miRNAs as repressors of gene expression, this review highlights their non-canonical novel role in the nucleus as activators or silencers of target gene transcription through miRNA-promoter interaction. The mechanistic details of the transcriptional role of miRNAs are yet to be elucidated, however, they can be explained by prospective models. In this review, we aim to discuss the different examples of transcriptional regulation by miRNAs and their possible mechanism of action, thereby offering a comprehensive perspective on the role of miRNAs in gene regulation and their importance in health and diseases.

MicroRNAs （miRNAs/miRs）是一种小的（长度为18-25个核苷酸）内源性非编码rna，通常通过与细胞质中靶mrna的3‘非翻译区（3’UTRs）相互作用来抑制基因表达。虽然大多数科学界仍然认为mirna是基因表达的抑制因子，但本综述强调了它们在细胞核中的非规范新作用，即通过mirna -启动子相互作用激活或沉默靶基因转录。mirna转录作用的机制细节尚未阐明。然而，它们可以用前瞻性模型来解释。在这篇综述中，我们旨在讨论mirna转录调控的不同例子及其可能的作用机制，从而提供mirna在基因调控中的作用及其在健康和疾病中的重要性的全面视角。

引用次数: 0

Long non-coding RNAs and their role in breast cancer pathogenesis and drug resistance: Navigating the non-coding landscape review 长链非编码rna及其在乳腺癌发病机制和耐药中的作用：导航非编码景观综述。

IF 3.3 3区生物学 Q3 CELL BIOLOGY

Experimental cell research

Pub Date : 2025-01-15 DOI: 10.1016/j.yexcr.2024.114365

Tohada M. Al-Noshokaty , Gharieb S. El-Sayyad , Rehab Abdelhamid , Abdallah Mansour , Nourhan Abdellatif , Ayat Alaaeldien , Tasnim Reda , David Gendi , Nourhan M. Abdelmaksoud , Shereen Saeid Elshaer , Ahmed S. Doghish , Osama A. Mohammed , Ahmed I. Abulsoud

Despite the progress made in the development of targeted therapies, breast cancer (BC) continues to pose a significant threat to the health of women. Transcriptomics has emerged due to the advancements in high-throughput sequencing technology. This provides crucial information about the role of non-coding RNAs (ncRNAs) in human cells, particularly long ncRNAs (lncRNAs), in disease development and function. When the control of these ncRNAs is disrupted, various illnesses emerge, including cancer. Numerous studies have produced empirical data on the function of lncRNAs in tumorigenesis and disease development. However, the roles and mechanisms of numerous lncRNAs remain unidentified at the molecular level because their regulatory role and the functional implications of abnormalities in cancer biology have yet to be thoroughly defined. The review gives an itemized summary of the most current developments in the role of lncRNA in BC, focusing on three main pathways, PI3K, MAPK, NF-kB, and hypoxia, and their resistance mechanisms.

尽管在开发靶向治疗方面取得了进展，但乳腺癌仍然对妇女的健康构成重大威胁。转录组学的出现是由于高通量测序技术的进步。这为人类细胞中非编码rna (ncRNAs)，特别是长链ncRNAs （lncRNAs）在疾病发展和功能中的作用提供了重要信息。当对这些ncrna的控制被破坏时，各种疾病就会出现，包括癌症。大量研究已经获得了lncrna在肿瘤发生和疾病发展中的作用的实证数据。然而，许多lncrna的作用和机制在分子水平上仍未被确定，因为它们在癌症生物学中的调节作用和异常的功能含义尚未被彻底定义。本文对lncRNA在BC中作用的最新进展进行了详细总结，重点介绍了PI3K、MAPK、NF-kB和缺氧这三个主要通路及其耐药机制。

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引用次数: 0

Interactions between lncRNAs and cyclins/CDKs complexes; key players in determining cancer cell response to CDKs inhibitors

IF 3.3 3区生物学 Q3 CELL BIOLOGY

Experimental cell research

Pub Date : 2025-01-04 DOI: 10.1016/j.yexcr.2025.114406

Bahaa Ibrahim Saeed , Abhinav Kumar , Enwa Felix Oghenemaro , Layla A. Almutairi , Rekha M. M , Rohit Kumawat , Subasini Uthirapathy , Hanen Mahmod Hulail , Shilpa Sharma , M. Ravi Kumar

Transcription takes place over a significant portion of the human genome. However, only a small portion of the transcriptome, roughly 1.2 %, consists of RNAs translated into proteins; the majority of transcripts, on the other hand, comprise a variety of RNA families with varying sizes and functions. A substantial portion of this diverse RNA universe consists of sequences longer than 200 bases, called the long non-coding RNA (lncRNA). The control of gene transcription, changes to DNA topology, nucleosome organization and structure, paraspeckle creation, and assistance for developing cellular organelles are only a few of the numerous tasks performed by lncRNA. The main focus of this study is on the function of lncRNA in controlling the levels and actions of cyclin-dependent kinase inhibitors (CDKIs). The enzymes required for the mitotic cycle's regulated progression are called cyclin-dependent kinases (CDKs). They have many degrees of regulation over their activities and interact with CDKIs as their crucial mechanisms. Interestingly, culminating evidence has clarified that lncRNAs are associated with several illnesses and use CDKI regulation to control cellular function. Nonetheless, despite the abundance of solid evidence in the literature, it still seems unlikely that lncRNA will have much of an impact on controlling cell proliferation or modulating CDKIs.

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引用次数: 0

Corrigendum to "Chronic hypoxia promotes pulmonary venous smooth muscle cell proliferation through the CaSR-TRPC6/ROCE pathway" [Exp. Cell Res. 2024 Dec 3;444(2):114363. doi: 10.1016/j.yexcr]. “慢性缺氧通过CaSR-TRPC6/ROCE通路促进肺静脉平滑肌细胞增殖”的修正[j] .细胞科学，2024,12月3日；444(2):114363。doi: 10.1016 / j.yexcr]。

IF 3.3 3区生物学 Q3 CELL BIOLOGY

Experimental cell research

Pub Date : 2025-01-01 DOI: 10.1016/j.yexcr.2024.114403

Shaoxing Li, Zhenli Fu, Wei Hong, Hong Yuan, Weitao Cao, Juan Xu, Rongmin Liu, Zhuandi Lin, Zhiming Xiang, Gongyong Peng

引用次数: 0

Corrigendum to "MOTS-c relieves hepatocellular carcinoma resistance to TRAIL-induced apoptosis under hypoxic conditions by activating MEF2A" [Exp. Cell Res., Volume 444, Issue 1, 1 January 2025, 114354]. “MOTS-c在低氧条件下通过激活MEF2A来缓解肝癌细胞对trail1诱导的凋亡的抵抗”[j].细胞研究，vol . 444, Issue 1, 2025, 114354。

IF 3.3 3区生物学 Q3 CELL BIOLOGY

Experimental cell research

Pub Date : 2024-12-21 DOI: 10.1016/j.yexcr.2024.114376

Haiying Shen, Junjie Nie, Xiaojun Wang, Guangqing Li, Liwei Zhao, Yuji Jin, Lianhai Jin

引用次数: 0