Cytotechnology最新文献

{"title":"cPLA₂α on the influence of Th17 and its role in the formation of liver fibrosis.","authors":"Lina Ma, Wei Wang, Limin Gu, Liyun Wang","doi":"10.1007/s10616-025-00750-6","DOIUrl":"10.1007/s10616-025-00750-6","url":null,"abstract":"<p><p>This study primarily investigated the mechanism and pathways of the cPLA₂α signaling pathway on Th17-mediated HSC activation and liver fibrosis, providing insights for clinical strategies to target HSC activation and delay the rapid progression of liver fibrosis. In vitro and in vivo model were established, and different concentrations of the cPLA₂α inhibitor AACOCF3 were administered respectively for intervention. The expression of IL- 17 was detected by ELISA, and the expression of cPLA₂α protein and HSC activation protein α-SMA index were detected by Western blot and immunofluorescence. In addition, observe the changes in the degree of liver fibrosis in mice through the pathological staining of mouse livers. In an in vitro system, Th17 could induce HSC activation. And after intervention, the results showed that the inhibitor could inhibit Th17 activation of HSC. Next, in an in vivo model, Th17 could also induce HSC activation. And after intervention, the results showed that the inhibitor could also inhibit HSC activation by Th17. Observation under liver pathological staining showed that the inflammation and staining were significantly reduced in the intervention group, suggesting a therapeutic effect of AACOCF3. Using in vitro and in vivo approaches, these data suggest that Th17 cells can promote the activation and proliferation of HSCs, which further exerts a role in promoting liver fibrosis. These data also suggest that the cPLA₂α pathway may be involved in the activation of HSCs by Th17 cells and induce liver fibrosis mechanisms.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"87"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11977053/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143969431","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}

{"title":"Huangqi Guizhi Wuwu decoction promoted the osteogenic differentiation of bone marrow mesenchymal stem cells by targeting ESR1.","authors":"Xin Zhao, Yanping Hu, Heran Xiong, Bo Dai, Wei Liu, Meiling Chen, Fan Zhou, Chao Xiang, Song Wang","doi":"10.1007/s10616-025-00773-z","DOIUrl":"10.1007/s10616-025-00773-z","url":null,"abstract":"<p><p>This study mainly explored the potential mechanism of Huangqi Guizhi Wuwu Decoction (HGWD) in the treatment of osteoarthritis (OA) based on network pharmacology, and to investigate whether HGWD promotes osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) by upregulating ESR1 based on in vitro experiments. The core target genes and potential signaling pathways related to HGWD in OA treatment were analyzed using network pharmacology analysis. BMSCs were isolated from rats to induce for adipogenic/osteogenic differentiation, which were assessed by Oil Red O staining and Alizarin Red staining, respectively. ESR1 knockdown lentivirus was transfected into BMSCs and different concentrations of rat HGWD-containing serum was prepared to treat BMSCs. Cell proliferation activity was measured by CCK-8 assay to select the optimal concentration for further experiments. Cells were treated with 10% HGWD-containing serum and transfected with ESR1 knockdown lentivirus. Osteogenic differentiation was assessed by ALP staining, ALP activity measurement, and Alizarin Red staining. The expression of osteogenic differentiation-related genes OCN, RUNX2, and COL1A1 was detected by qRT-PCR and Western blot. Network pharmacology analysis revealed that ESR1 is one of the core targets of HGWD in OA treatment. HGWD-containing serum promoted proliferation and osteogenic differentiation ability of BMSCs, and also increased ESR1 expression. The promoting effects of HGWD-containing serum on proliferation and osteogenic differentiation were partially polished in response to ESR1 knockdown in BMSCs. Based on the collective evidence, the therapeutic effects of HGWD in OA may be achieved by promoting osteogenic differentiation of BMSCs via upregulating ESR1 expression.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00773-z.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"110"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12119448/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144198418","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}

{"title":"Cell-based evaluation of anti-inflammatory activity from the combination of natural compounds in LPS-stimulated U937 monocytes.","authors":"Maria Giovanna Rizzo, Cristiana Roberta Multisanti, Caterina Faggio, Federica Impellitteri","doi":"10.1007/s10616-025-00788-6","DOIUrl":"10.1007/s10616-025-00788-6","url":null,"abstract":"<p><p>The present study aims to examine the potential effects of a novel coupling of natural-derived compounds modulating inflammatory responses. Their effects were assessed in LPS-inflamed U937 pro-monocytes. Monocytes were exposed to incremental concentrations of citric acid (2-hydroxy-1, 2, 3-propanetricarboxylic acid) and quercetin (3, 3', 4', 5, 7-pentahydroxyflavone), administered individually and in combination. Evaluation of cell viability was conducted via the MTT assay; nitric oxide (NO) production was assessed using the Griess assay; the expression levels of key pro-inflammatory markers (IL-1β, IL-6, TNF-α, and COX-2) were determined through quantitative real-time PCR (qRT-PCR). The results indicate that the two combined substances modulate the pathways of anti-inflammatory cytokines in pro-monocytic cells. Collectively, our data indicated that the synergistic activity of quercetin and citric acid has the potential to be developed as a novel therapeutic agent for inflammatory-related diseases, also opening new avenues for developing natural strategies in pathologies related to inflammatory processes treatment.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"117"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12145369/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144257522","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}

{"title":"Mechanism of the N6-methyladenosine reader heterogeneous nuclear ribonucleoprotein C facilitating immune escape in thyroid cancer by stabilizing programmed death ligand 1.","authors":"Nuoxuan Li, Liang Wang, Jie Yao, Hong Yang","doi":"10.1007/s10616-025-00755-1","DOIUrl":"10.1007/s10616-025-00755-1","url":null,"abstract":"<p><p>Thyroid cancer (TC) is a leading malignancy of the endocrine system. We investigated mechanism of the N6-methyladenosine (m6A) reader heterogeneous nuclear ribonucleoprotein C (HNRNPC) facilitating immune escape in TC by stabilizing programmed death ligand 1 (PD-L1). HNRNPC expression in TC tissues was analyzed using databases. Human TC cells (BHT-101, B-CPAP, SW579) and human thyroid follicular epithelial cells (Nthy-ori3-1) were cultured in vitro. SW579 cells were treated with pcDNA3.1-HNRNPC (oe-HNRNPC) and small interfering (si)-PD-L1, and B-CPAP cells were transfected with si-HNRNPC. HNRNPC and PD-L1 expression levels were assessed by RT-qPCR and Western blot. Cell proliferation, migration and invasion were evaluated by CCK-8, colony formation, and Transwell assays. Carboxyfluorescein diacetate succinimidyl ester-labelled CD8⁺ T cell proliferation and effector cytokine (interferon-γ, tumor necrosis factor-α) levels were measured by flow cytometry and ELISA. The correlation between HNRNPC and PD-L1 expression in TC tissues, m6A modification sites on PD-L1 messenger RNA (mRNA), and HNRNPC-PD-L1 interaction were analyzed by databases and RIP assay. PD-L1 m6A modification was determined by Me-RIP assay. PD-L1 mRNA stability was detected by treating cells with actinomycin D. HNRNPC was notably highly expressed in TC cells. HNRNPC promoted TC cell proliferation, migration and invasion, facilitating immune escape. Mechanistically, HNRNPC mediated m6A modification to strengthen PD-L1 mRNA stability and up-regulate PD-L1 expression. Moreover, knockdown of PD-L1 partially reversed the promotional effect of HNRNPC on immune escape in TC cells. HNRNPC bolstered PD-L1 stability and up-regulated PD-L1 expression through m6A modification, thus promoting immune escape in TC.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"96"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12055676/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143978502","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}

{"title":"Catalpol inhibits Hedgehog signaling pathway to suppress proliferation and promote lipid accumulation in rat meibomian gland epithelial cells.","authors":"Zibin Liu, Rui Zhang, Jian Lai","doi":"10.1007/s10616-025-00769-9","DOIUrl":"10.1007/s10616-025-00769-9","url":null,"abstract":"<p><p>Meibomian gland dysfunction (MGD) is an ocular surface disease lacking optimal treatment strategy. The Hedgehog pathway is involved in regulating MGEC proliferation and differentiation. Catalpol (CAT) is the main active ingredient in <i>Rehmannia glutinosa</i> with therapeutic potential. Exploring the effects and biological mechanisms of CAT on meibomian gland epithelial cells (MGECs). Primarily cultured rat MGECs were co-cultured with 3T3 cells for 7 days. MGECs were exposed to 2.5, 5, and 10 mmol/L CAT, 10 μg/mL Azithromycin (AZM), and 0.6 μmol/L Smoothened receptor agonist (SAG) for 48 h. Colony formation assays, Cell counting kit-8, Ki67 immunofluorescence, Nile red and Oil red O staining, and HSD LipidTOX Green kits were used to assess cell proliferation and lipid accumulation. Real-time quantitative PCR and Western blot analysis were used to measure gene expressions related to Hedgehog- and peroxisome proliferator-activated receptor (PPAR)-γ. This study successfully isolated primarily rat MGECs (expressed P63 and K14). AZM and 5, and 10 mmol/L CAT inhibited colony number, cell viability, and Ki67 mean fluorescence intensity (MFI), while they enhanced MFI of Nile red and LipidTOX Green, as well as increasing the ratio of Oil red O staining area. Additionally, transcription and translation levels of the Hedgehog pathway were significantly suppressed, meanwhile, PPAR-γ and SREBP-1 expression were increased. Interestingly, SAG reversed the effects of 10 mmol/L CAT on MGECs. CAT suppresses MGEC proliferation and promotes lipid accumulation by inhibiting the Hedgehog signaling pathway. This study offers a potential therapeutic strategy for MGD.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00769-9.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"105"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12092864/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144126962","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}

{"title":"Icariside II inhibits gastric cancer progression by suppressing the Wnt/β-catenin signaling pathway.","authors":"Rongrong Dou, Xiaowei Zhu, Xinyun Liu, Jingjing Bao, Rongrong Jin, Guangyao Mao, Hong Yu, Yifei Liu","doi":"10.1007/s10616-025-00761-3","DOIUrl":"10.1007/s10616-025-00761-3","url":null,"abstract":"<p><p>Gastric cancer is one of the common malignant tumours in clinical practice with poor prognosis and high mortality. Icariside II is a single compound extracted from the traditional Chinese medicine <i>Epimedium brevicornu</i> Maxim, and it is also the main active ingredient of <i>Epimedium brevicornu</i> Maxim that exerts pharmacological effects. Studies have shown that Icariside II has anti-tumour activity, but its mechanism of action on gastric cancer cells is unclear. This study aims to analyze the impact of Icariside II on gastric cancer cells as well as on xenograft tumor models of gastric cancer, and to examine the potential molecular regulatory pathways. GES-1, a normal gastric cell line, and gastric cancer cell lines AGS and MGC803 were cultured to investigate the cytotoxic effects of Icariside II using the methylthiazolyldiphenyl-tetrazolium (MTT). Flow cytometry (FCM) was employed to measure the impact of Icariside II on the apoptosis levels of gastric cancer cells, while western blot analysis was used to examine the expression of apoptosis-related proteins and the Wnt/β-catenin signaling pathway. Subsequently, a xenograft tumor model was established and treated with Icariside II to observe changes in tumor volume and weight in the model mice. Finally, alterations in the expression of the Wnt/β-catenin signaling pathway were assessed through immunofluorescence (IF) and immunohistochemistry (IHC). The results showed that Icariside II had faint significant toxic effect on GES-1 cells, and was able to inhibit the proliferative activity and promote apoptosis of the gastric cancer cells. Moreover, Icariside II was able to inhibit the growth of gastric cancer in nude mice subcutaneous transplantation tumor. In addition, both in vivo and in vitro results indicated that Icariside II inhibited the activation of the Wnt/β-catenin signaling pathway. Icariside II inhibited tumorigenicity of gastric cancer by suppressing the Wnt/β-catenin signaling.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"106"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12098252/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144141789","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}

{"title":"Green synthesis and characterization of zinc oxide nanoparticles using <i>Vitex negundo</i> methanolic extract and its anticancer efficacy in colorectal cancer.","authors":"Kumaresan Kowsalya, Gayathiri Gunasangkaran, Jayachandran Halka, Eswaramoorthy Dharani, Muthukrishnan Saradhadevi, Arumugam Vijaya Anand, Muthukrishnan Anand, Packiaraj Gurusaravanan, Giridharan Bupesh, Muthukrishnan Arun","doi":"10.1007/s10616-025-00775-x","DOIUrl":"10.1007/s10616-025-00775-x","url":null,"abstract":"<p><p><i>Vitex negundo</i> is a traditional medicinal plant known for its anticancer properties, particularly its effectiveness in targeting apoptosis-related cancer pathways. Colorectal cancer is the most prevalent malignancy worldwide, often requiring alternative therapies involving plant-derived bioactive compounds. This study aimed to synthesize zinc oxide nanoparticles using <i>V. negundo</i> leaves (VnZnONP) and confirm their formation through characterization studies. Further, the anticancer efficacy of VnZnONPs was also evaluated in HT-29 colorectal cancer cells. Zinc oxide nanoparticles were synthesized using methanolic leaf extract of <i>V. negundo</i> (MeVn), which contained nearly 39 phytocompounds, identified in gas chromatography-mass spectrometry (GC-MS). UV-vis spectroscopy showed a prominent peak at 374 nm, while dynamic light scattering (DLS) revealed a size distribution peaking at 452.5 nm. In SEM analysis, the spherical-shaped morphology with random distribution was observed. EDX analysis confirmed the presence of zinc and oxygen, and zeta potential analysis showed a + 41.4 mV charge, indicating stable nanoparticles. FTIR analysis identified functional groups such as aliphatic, aromatic compounds, alkenes, alcohols, and amides. In the DPPH assay, VnZnONP at 100 µg/ml exhibited 87.96% antioxidant activity, significantly higher than MeVn (39.89%). VnZnONPs showed dose-dependent cytotoxicity against HT-29 cells with an IC₅₀ value of 60.56 µg/ml. In addition, DAPI staining confirmed nuclear damage, and acridine orange/ethidium bromide staining indicated early and late apoptosis. RT-PCR analysis revealed downregulation of <i>Jab1</i> and <i>Bcl2</i>, and upregulation of <i>Bax</i>, <i>Caspase-3</i>, and <i>Caspase-9</i>. This study demonstrates that <i>V. negundo</i>-based ZnO nanoparticles can promote apoptosis and can serve as a promising therapeutic agent for colorectal cancer.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00775-x.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"112"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12125431/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144198376","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}

{"title":"Mechanisms of CRLF3-targeted binding to ACTR2 to promote hepatocellular carcinoma progression and effects on the immune microenvironment.","authors":"SuSu Ye, XinLei Zhang, FengChao Liu, QingHui Niu, AiLing Liu, Di Xia","doi":"10.1007/s10616-025-00780-0","DOIUrl":"10.1007/s10616-025-00780-0","url":null,"abstract":"<p><p>This study aimed to delve deeper into the effects of CRLF3 on the immune microenvironment and the interaction between CRLF3 and ACTR2 in hepatocellular carcinoma (HCC). CRLF3 and ACTR2 in mouse tumor tissues and HepG2 cells were measured by RT-qPCR and Western Blot. The proliferative ability of HepG2 cells was assessed by MTT and colony formation assays, with apoptosis determined by flow cytometry, and migration and invasion quantified by Transwell assay. The apoptosis rate of CD8⁺ T cells was calculated by flow cytometry, as well as TNF-α and IFN-γ positivity in CD8⁺ T cells. TNF-α, IFN-γ, and IL-2 were assayed by ELISA. The interaction between CRLF3 and ACTR2 was examined using immunoprecipitation and Western Blot experiments. CRLF3 targeted binding to ACTR2 promoted the proliferative and migratory capacities of HepG2 cells and inhibited apoptosis. Lowering CRLF3 inhibited HCC cell immune escape, with a significant increase in TNF-α and IFN-γ-positive populations in CD8⁺ T cells, and enhancing ACTR2 significantly mitigated this effect. Lowering CRLF3 inhibited HCC xenografted tumor growth in nude mice. Through its targeted binding to ACTR2, CRLF3 aids in the growth and immune escape of HCC cells.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"113"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12130405/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144224647","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}

{"title":"Correction: PABPC1 silencing inhibits pancreatic cancer cell proliferation and EMT, and induces apoptosis via PI3K/AKT pathway.","authors":"Changren Zhu, Cuimei Wang, Xiaodong Wang, Shuangshuang Dong, Qing Xu, Jun Zheng","doi":"10.1007/s10616-025-00760-4","DOIUrl":"10.1007/s10616-025-00760-4","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1007/s10616-024-00626-1.].</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"98"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12075723/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075918","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}

{"title":"Correction: Mechanism underlying the role of the circRNA OMA1/miR-654-3p/RAF1 axis in children with inflammatory bowel disease.","authors":"Ping Zhang, Zhenhui Wang, Yufen Xu, Meirong Wu","doi":"10.1007/s10616-025-00770-2","DOIUrl":"10.1007/s10616-025-00770-2","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1007/s10616-025-00703-z.].</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"109"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12119397/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144198375","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}