Acta biochimica et biophysica Sinica最新文献_第3页

Exosomal integrin alpha 3 promotes epithelial ovarian cancer cell migration via the S100A7/p-ERK signaling pathway.

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-03-07 DOI: 10.3724/abbs.2025024

Zeyuan Yin, Jiachen Ma, Joseph Adu-Amankwaah, Guangyan Xie, Yinghao Wang, Wei Tai, Zhenquan Sun, Chuting Huang, Guanfeng Chen, Tong Fu, Bei Zhang, Xueyan Zhou

{"title":"Exosomal integrin alpha 3 promotes epithelial ovarian cancer cell migration via the S100A7/p-ERK signaling pathway.","authors":"Zeyuan Yin, Jiachen Ma, Joseph Adu-Amankwaah, Guangyan Xie, Yinghao Wang, Wei Tai, Zhenquan Sun, Chuting Huang, Guanfeng Chen, Tong Fu, Bei Zhang, Xueyan Zhou","doi":"10.3724/abbs.2025024","DOIUrl":"https://doi.org/10.3724/abbs.2025024","url":null,"abstract":"Epithelial ovarian cancer (EOC) is a highly aggressive malignancy with a poor prognosis due to late-stage diagnosis and the lack of reliable biomarkers for early detection. Exosomes, small vesicles involved in intercellular communication, play a critical role in cancer progression by promoting migration, proliferation, and metastasis. This study investigates the role of exosomal proteins in EOC cell migration and identifies potential biomarkers. Exosomes are isolated from the ascites fluid of EOC patients (C-Exos) and benign ovarian disease patients (B-Exos), and mass spectrometry analysis of clinical samples reveals 185 differentially expressed proteins, with integrin alpha 3 (ITGA3) being strongly associated with poor prognosis. ITGA3 is transported via exosomes to recipient EOC cells, where it is released into the cytoplasm and translocated to the cell membrane. This localization enables ITGA3 to activate the intracellular signaling pathways that drive EOC migration. Immunoprecipitation mass spectrometry of clinical samples reveals that ITGA3 may influence EOC migration through the S100A7/p-ERK signaling pathway. Mechanistically, ITGA3 activates ERK signaling through S100A7, promoting cell migration. In vivo, exosomes enrich with ITGA3 facilitates tumor growth and migration, whereas ITGA3 knockdown reduces these effects. These findings suggest that exosomal ITGA3, via the S100A7/p-ERK signaling pathway, promotes EOC cell migration. ITGA3 could serve as a prognostic biomarker and therapeutic target in EOC. Targeting the ITGA3/S100A7 axis may help suppress migration, suggesting a promising strategy to improve EOC patient outcomes.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Gastrodin inhibits reactive astrocyte-mediated inflammation in hypoxic-ischemic brain damage through S100B/RAGE-Smad3 signaling.

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-03-07 DOI: 10.3724/abbs.2024235

Pengxiang Wang, Hanjun Zuo, Haolong Shi, Zhao Wang, Xueqi Ren, Jinsha Shi, Tao Guo, Xianfeng Kuang, Min Zhao, Jinghui Li, Juanjuan Li

{"title":"Gastrodin inhibits reactive astrocyte-mediated inflammation in hypoxic-ischemic brain damage through S100B/RAGE-Smad3 signaling.","authors":"Pengxiang Wang, Hanjun Zuo, Haolong Shi, Zhao Wang, Xueqi Ren, Jinsha Shi, Tao Guo, Xianfeng Kuang, Min Zhao, Jinghui Li, Juanjuan Li","doi":"10.3724/abbs.2024235","DOIUrl":"https://doi.org/10.3724/abbs.2024235","url":null,"abstract":"Activated astrocytes and their associated inflammatory responses play critical roles in the pathogenesis of hypoxic-ischemic brain damage (HIBD). Gastrodin (GAS), an anti-inflammatory herbal agent, is known to suppress microglial activation. Here, we investigate whether it exerts a similar effect on activated astrocytes and whether it acts through S100B/RAGE-Smad3 signaling. The expression changes of S100B/RAGE-Smad3 signaling pathway-related proteins, inflammatory factors and A1/A2 astrocyte markers were detected by ELISA, western blot analysis, immunofluorescence and immunohistochemistry. The results show that GAS decreases the expression of sRAGE in the brain tissue and S100B in the serum and brain tissue of HIBD mice. However, it promotes the expression of sRAGE in the serum of HIBD mice. Moreover, GAS inhibits the expressions of RAGE, p-Smad3, TNF-α, and C3 (A1 astrocyte marker), and promotes the expressions of S100A10 (A2 astrocyte marker) and BDNF in HIBD model mice, as well as in oxygen glucose deprivation (OGD)-treated TNC-1 astrocytes. The immunofluorescence and immunohistochemical results of RAGE and p-Smad3, as well as the immunofluorescence results of C3 and S100A10, reveal the same trend. Interestingly, FPS-ZM1 (a specific inhibitor of RAGE) inhibits the expressions of p-Smad3, TNF-α, C3, and S100A10, but promotes that of BDNF compared with those in the OGD group. The combination of GAS and FPS-ZM1 further decreases the expression of C3. These results indicate that GAS can inhibit the activation of Smad3 through S100B/RAGE signaling and regulate the expression of A1/A2-type astrocytes.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

circ_0000389 inhibits intervertebral disc degeneration by targeting the miR-346/KLF7 axis.

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-03-07 DOI: 10.3724/abbs.2025029

Chun Liu, Cheng Yu, Yang Duan, Jianjun Li, Xiang Chen, Wenning Xu, Sujun Qiu

{"title":"circ_0000389 inhibits intervertebral disc degeneration by targeting the miR-346/KLF7 axis.","authors":"Chun Liu, Cheng Yu, Yang Duan, Jianjun Li, Xiang Chen, Wenning Xu, Sujun Qiu","doi":"10.3724/abbs.2025029","DOIUrl":"https://doi.org/10.3724/abbs.2025029","url":null,"abstract":"Intervertebral disc degeneration (IVDD) is a major cause of low back pain. An increasing number of studies have demonstrated that circRNAs regulate the progression of IVDD. However, the specific role of circ_0000389 in the progression of IVDD is not clear. In this study, circ_0000389 is selected by bioinformatics analysis of the GSE67566 dataset. RT-qPCR is performed to detect the expressions of circ_0000389, miR-346 and KLF7 in nucleus pulposus (NP) tissues. The proliferative capacity of nucleus pulposus cells (NPCs) is examined via CCK-8 assay. Western blot analysis of extracellular matrix (ECM) catabolism is performed in NPCs. Dual-luciferase reporter gene assays and RNA immunoprecipitation (RIP) confirm the interaction of circ_0000389 with miR-346 and KLF7. The expression of circ_0000389 is significantly downregulated in degenerating NP tissues. Functionally, circ_0000389 inhibits ECM catabolism. Mechanistically, we identify miR-346 and KLF7 as downstream target genes of circ_0000389 and miR-346, respectively. miR-346 overexpression reverses the effect of circ_0000389 on NPCs, and KLF7 overexpression reverses the effect of miR-346 on NPCs, indicating that circ_0000389 alleviates IVDD progression by regulating the miR-346/KLF7 axis. This study may provide a new therapeutic target for the treatment of IVDD.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

ISGylation: is our genome yearning for such a modification?

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-02-28 DOI: 10.3724/abbs.2025028

Zheng Chen, Zheng Li, Ying Wang, Zaure Dushimova, Kapanova Gulnara, Shunichi Takeda, Zhongjun Zhou, Xingzhi Xu

引用次数: 0

p53-dependent chromatin relaxation is required for DNA double-strand break repair.

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-02-26 DOI: 10.3724/abbs.2025008

Hongyu Chen, Jin Shan, Wenjing Qi, Lili Chen, Xianlu Zeng

{"title":"p53-dependent chromatin relaxation is required for DNA double-strand break repair.","authors":"Hongyu Chen, Jin Shan, Wenjing Qi, Lili Chen, Xianlu Zeng","doi":"10.3724/abbs.2025008","DOIUrl":"https://doi.org/10.3724/abbs.2025008","url":null,"abstract":"The tumor suppressor p53, an indispensable nuclear transcription factor, plays a central role in orchestrating cellular responses when DNA damage occurs. In this study, we demonstrate that in the initial phases of DNA double-strand break (DSB) repair, p53 is rapidly recruited to sites of damage and the surrounding chromatin, where it enhances DSB repair efficiency. This enhancement occurs through the modulation of chromatin dynamics and the promotion of a more relaxed chromatin configuration, a process influenced by p53 in response to DSB-inducing factors such as etoposide, ultraviolet radiation, and nucleases. These results underscore the pivotal function of p53 as a rapid responder to DSBs, delineating a significant departure from its traditionally recognized role as a downstream transcriptional regulator in DNA damage repair processes. This study emphasizes that the direct engagement of p53 in DNA repair through chromatin structure regulation extends beyond its established involvement in UV irradiation-induced nucleotide excision repair (NER), demonstrating analogous mechanistic attributes in the context of DSB repair. This newly illuminated perspective enhances our understanding of the multifaceted roles of p53 in genome stability and integrity.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143497492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

The combination of fatigue with the serum GCSF improves the performance of serological screening for frailty.

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-02-26 DOI: 10.3724/abbs.2025007

Jiaming Yu, Jie Chen, Xueying Ji, Yixuan Qiu, Yan Zhang, Jiaofeng Wang, Xiangqi Li, Chaobao Zhang, Zhijun Bao

引用次数: 0

Corrigendum to: Downregulating integrin subunit alpha 7 (ITGA7) promotes proliferation, invasion, and migration of papillary thyroid carcinoma cells through regulating epithelial-to-mesenchymal transition. 下调整合素亚单位α 7 （ITGA7）可通过调节上皮细胞向间质细胞的转变促进甲状腺乳头状癌细胞的增殖、侵袭和迁移。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-02-25 DOI: 10.3724/abbs.2024200

Yaoyao Guan, Adheesh Bhandari, Erjie Xia, Lingguo Kong, Xiaohua Zhang, Ouchen Wang

引用次数: 0

Corrigendum to: HSPA8-mediated stability of the CLPP protein regulates mitochondrial autophagy in cisplatin-resistant ovarian cancer cells. hspa8介导的CLPP蛋白的稳定性调节顺铂耐药卵巢癌细胞的线粒体自噬。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-02-25 DOI: 10.3724/abbs.2024243

Xinxin Kou, Xiaoxia Yang, Zheng Zhao, Lei Li

引用次数: 0

KAT8 facilitates the proliferation of cancer cells through enhancing E7 function in HPV-associated cervical cancer.

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-02-24 DOI: 10.3724/abbs.2025022

Anli Xu, Xiaoming Yang, Junwei Zhao, Shujun Kong, Qing Tang, Xiangzhi Li, Hongmei Qu, Guoyun Wang

{"title":"KAT8 facilitates the proliferation of cancer cells through enhancing E7 function in HPV-associated cervical cancer.","authors":"Anli Xu, Xiaoming Yang, Junwei Zhao, Shujun Kong, Qing Tang, Xiangzhi Li, Hongmei Qu, Guoyun Wang","doi":"10.3724/abbs.2025022","DOIUrl":"https://doi.org/10.3724/abbs.2025022","url":null,"abstract":"Persistent human papillomavirus (HPV) infection serves as the principal etiological factor in cervical cancer, with the oncoprotein E7, which is encoded by the virus, playing a key role in tumorigenesis. However, targeted therapeutic strategies against E7 remain underexplored. KAT8, a lysine acetyltransferase, significantly contributes to oncogenesis through the regulation of transcription. However, its involvement in cervical cancer remains inadequately characterized. This study employs HPV18-positive HeLa and HPV16-positive SiHa cell lines to investigate how KAT8 modulates E7 expression and function in cervical cancer cells. Upon KAT8 knockdown, a marked reduction in cell viability is observed, alongside a decrease in E7 expression. This is associated with elevated level of retinoblastoma protein (pRb) and decreased E2F1 expression, indicating that KAT8 depletion inhibits E7 expression, resulting in E2F1 inactivation and cell cycle arrest. Furthermore, KAT8 directly binds to the promoter regions of the HPV18 LCR, enhancing the transcription of the HPV18 E7 gene. This study also demonstrates that KAT8 is essential for the acetylation of E7 and plays a critical role in facilitating the interaction between pRb/E2F1 and E7 in cervical cancer cells. In conclusion, these results highlight KAT8 as a key driver of cervical cancer progression, promoting the expression of HPV E7 and its associated oncogenic signaling pathways.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143482001","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Divergent roles of PKM2 in regulating PD-L1 and PD-L2 expression and their implications in human and mouse cancer models.

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2025-02-21 DOI: 10.3724/abbs.2025019

Shuo He, Shujuan Luo, Bangwu Cai, Jiao Chen, Yao Zhang, Feng Zhao, Qing Liu, Tao Liu, Wei Wang, Tianyuan Peng, Xiaomei Lu, Shutao Zheng

{"title":"Divergent roles of PKM2 in regulating PD-L1 and PD-L2 expression and their implications in human and mouse cancer models.","authors":"Shuo He, Shujuan Luo, Bangwu Cai, Jiao Chen, Yao Zhang, Feng Zhao, Qing Liu, Tao Liu, Wei Wang, Tianyuan Peng, Xiaomei Lu, Shutao Zheng","doi":"10.3724/abbs.2025019","DOIUrl":"https://doi.org/10.3724/abbs.2025019","url":null,"abstract":"Cancer cells evade immune detection through checkpoint molecules like PD-L1 and PD-L2 which suppress T-cell activation. While PD-L1 is well-studied, the role of PD-L2 remains unclear. Pyruvate kinase M2 (PKM2), a metabolic enzyme, influences immune checkpoint regulation, but its role in PD-L1 and PD-L2 modulation is not well defined. Here, we investigate the role of pyruvate kinase M2 (PKM2) in modulating the immune checkpoint molecules PD-L1 and PD-L2 via GATA3 in cancer cells, with insights from both human and mouse models. We find that PKM2 enhances PD-L1 expression while inhibiting PD-L2, a dual regulatory mechanism that facilitates immune evasion. Knockdown and overexpression experiments revealed GATA3 as a key mediator. PKM2 knockout reduced GATA3 level, leading to decreased PD-L1 and increased PD-L2 expression. Chromatin immunoprecipitation (ChIP)-qPCR demonstrates that GATA3 functions as a direct transcription factor capable of binding to the promoters of PD-L1 and PD-L2. In silico analyses of 81 esophageal squamous cell carcinoma (ESCC) cases from the TCGA database demonstrate that PKM2 mRNA is unrelated to PD-L1 and PD-L2 expression but is negatively correlated with CD8 + T-cell infiltration in ESCC. To further validate these findings, we establish a xenograft model using immune-competent C57/BL6N mice, where knockdown of PKM2 results in significant downregulation of both PD-L1 and PD-L2 expression. Collectively, these findings underscore the divergent roles of PKM2 in regulating immune checkpoint expression in human and mouse cancer models and suggest that targeting the PKM2-GATA3 axis could enhance cancer immunotherapy by fine-tuning PD-L1 and PD-L2 levels.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143466627","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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