Journal of Cell Communication and Signaling最新文献_第9页

Role for CCN1 in lysophosphatidic acid response in PC-3 human prostate cancer cells CCN1 在 PC-3 人类前列腺癌细胞的溶血磷脂酸反应中的作用

IF 4.1 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2024-02-20 DOI: 10.1002/ccs3.12019

Pravita Balijepalli, Brianna K. Knode, Samuel A. Nahulu, Emily L. Abrahamson, Mary P. Nivison, Kathryn E. Meier

{"title":"Role for CCN1 in lysophosphatidic acid response in PC-3 human prostate cancer cells","authors":"Pravita Balijepalli, Brianna K. Knode, Samuel A. Nahulu, Emily L. Abrahamson, Mary P. Nivison, Kathryn E. Meier","doi":"10.1002/ccs3.12019","DOIUrl":"https://doi.org/10.1002/ccs3.12019","url":null,"abstract":"<p>Lysophosphatidic acid (LPA) and sphingosine 1-phosphate (S1P) are bioactive phospholipids that act as mitogens in various cancers. Both LPA and S1P activate G-protein coupled receptors (GPCRs). We examined the role of CCN1/CYR61, an inducible matricellular protein, in LPA-induced signal transduction in PC-3 human prostate cancer cells. We found that both LPA and S1P induced expression of CCN1 and CCN2 within 2–4 h. CCN1 was induced by 18:1-LPA, but not by 18:0-, 18:2-, or 18:3-LPAs. A free fatty acid receptor-4 agonist inhibited LPA-induced CCN1 induction. CCN1 appeared in the ECM within 2 h after LPA addition. LPA caused biphasic activation of Erk MAPK, with an initial peak at 10–20 min followed by a later phase after 6 h. LPA increased adhesion of PC-3 cells to culture substrates (standard culture plates, fibronectin, or extracellular matrix) at 2 h, an intermediate event between early and late LPA signals. Knockdown of CCN1 suppressed LPA-induced adhesion to ECM or fibronectin. ECM from CCN1 knockdown cells was a poor substrate for adhesion, as compared to ECM from control cells. These results suggest that CCN1 contributes to LPA responses in the tumor microenvironment. The LPA-CCN1 axis holds promise for the development of novel therapeutic strategies in cancer.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2024-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.12019","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140104540","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

Lactate drives CD38 signaling to promote Epithelial-Mesenchymal Transition through Snail induction in non-small cell lung cancer cells 乳酸盐通过蜗牛诱导CD38信号传导，促进非小细胞肺癌细胞的上皮-间质转化

IF 4.1 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2024-02-14 DOI: 10.1002/ccs3.12018

Yating Lu, Yang Yang, Tao Chang, Qiyun Jiang, Chenfeng Yang, Chunzhe Fu, Huijun Wei, Yuanpeng He, Zhihao Wu

引用次数: 0

IncRNA AC004943.2 regulates miR-135a-5p and PTK2/P13K axis to promote laryngeal squamous cell carcinoma progression IncRNA AC004943.2调控miR-135a-5p和PTK2/P13K轴，促进喉鳞状细胞癌进展

IF 4.1 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2024-02-09 DOI: 10.1002/ccs3.12016

Xiaowen Zhu, Wenming Dong, Meijia Zhang

{"title":"IncRNA AC004943.2 regulates miR-135a-5p and PTK2/P13K axis to promote laryngeal squamous cell carcinoma progression","authors":"Xiaowen Zhu, Wenming Dong, Meijia Zhang","doi":"10.1002/ccs3.12016","DOIUrl":"10.1002/ccs3.12016","url":null,"abstract":"<p>Long noncoding RNAs (lncRNAs) are involved in regulatory processes in laryngeal squamous cell carcinoma (LSCC) at posttranscriptional epigenetic modification level. Yet, the function and underlying mechanism behind lncRNA AC004943.2 in LSCC is still obscure. Therefore, the potential role of AC004943.2 in LSCC progression was investigated. The expression of gene or protein was tested by real-time quantitative polymerase chain reaction and western blot. MTT, colony formation, wound healing, and transwell experiments were applied to detect LSCC cell viability, proliferation, migration and invasion, respectively. The interaction among AC004943.2, miR-135a-5p, and protein tyrosine kinase 2 (PTK2) were analyzed by bioinformatics prediction and luciferase assay. AC004943.2 was highly expressed in LSCC cells compared with normal human bronchial epithelial cells, while miR-135a-5p was lowly expressed. AC004943.2 knockdown or miR-135a-5p overexpression inhibited LSCC cell viability, proliferation, migration and invasion. Mechanistically, AC004943.2 increased PTK2 expression in LSCC cells by sponging miR-135a-5p. Furthermore, miR-135a-5p knockdown inverted the inhibitory effect of AC004943.2 silencing on LSCC cell malignant behaviors. MiR-135a-5p upregulation attenuated the PTK2/PI3K pathway to inhibit progression of LSCC. AC004943.2 facilitated the cancerous phenotypes of LSCC cells by activating the PTK2/PI3K pathway through targeting miR-135a-5p, which furnished a therapeutic candidate for LSCC treatment.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2024-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.12016","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139789559","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

JAK3/STAT5 signaling-triggered upregulation of PIK3CD contributes to gastric carcinoma development JAK3/STAT5 信号触发的 PIK3CD 上调有助于胃癌的发展

IF 4.1 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2024-02-07 DOI: 10.1002/ccs3.12017

Qingqing Hu, Ning Dou, Qiong Wu, Yong Gao, Yandong Li, Jingde Chen

{"title":"JAK3/STAT5 signaling-triggered upregulation of PIK3CD contributes to gastric carcinoma development","authors":"Qingqing Hu, Ning Dou, Qiong Wu, Yong Gao, Yandong Li, Jingde Chen","doi":"10.1002/ccs3.12017","DOIUrl":"10.1002/ccs3.12017","url":null,"abstract":"<p>Gastric cancer (GC) is one of the most common solid cancers with high incidence and mortality worldwide. Chronic gastritis and consequent inflammatory microenvironment is known as a major cause leading to gastric carcinogenesis. Here we report that PIK3CD that encodes p110δ, a catalytic subunit of the class IA PI3Ks, is overexpressed and tumorigenic in GC and associated with tumor inflammatory microenvironment. By investigating the data from TCGA database and our immunohistochemical staining and quantitative real-time PCR results from clinical samples, we found PIK3CD exhibits higher expression level in GC tissues compared with adjacent non-tumorous stomach tissues. Genetic silencing of PIK3CD in GC cells retards proliferation and migration in vitro and tumorigenicity and metastasis in vivo. In contrast, enhanced expression of PIK3CD promotes these phenotypes in vitro. Furthermore, pharmacological inhibition of PIK3CD could reduce GC cell viability and colony formation capacities. More importantly, we reveal a relevant mechanism that PIK3CD, but not PIK3CA and PIK3CB, is transcriptionally regulated by the pro-inflammatory IL2/JAK3/STAT5 axis and tumor-infiltrating immune cells such as lymphocytes. These observations may setup a new crosstalk between tumor inflammatory microenvironment, IL2/JAK3/STAT5 signaling and PI3K/AKT signaling. Targeting PIK3CD may be a promising therapy strategy for GC.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2024-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.12017","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139795808","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

Survivin inhibition ameliorates liver fibrosis by inducing hepatic stellate cell senescence and depleting hepatic macrophage population 抑制 Survivin 可通过诱导肝星状细胞衰老和消耗肝巨噬细胞数量来改善肝纤维化

IF 4.1 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2024-01-25 DOI: 10.1002/ccs3.12015

Sachin Sharma, Shaikh Maryam Ghufran, Mehreen Aftab, Chhagan Bihari, Sampa Ghose, Subhrajit Biswas

{"title":"Survivin inhibition ameliorates liver fibrosis by inducing hepatic stellate cell senescence and depleting hepatic macrophage population","authors":"Sachin Sharma, Shaikh Maryam Ghufran, Mehreen Aftab, Chhagan Bihari, Sampa Ghose, Subhrajit Biswas","doi":"10.1002/ccs3.12015","DOIUrl":"10.1002/ccs3.12015","url":null,"abstract":"<p>Persistent activation of hepatic stellate cells (HSCs) in the injured liver leads to the progression of liver injury from fibrosis to detrimental cirrhosis. In a previous study, we have shown that survivin protein is upregulated during the early activation of HSCs, which triggers the onset of liver fibrosis. However, the therapeutic potential of targeting survivin in a fully established fibrotic liver needs to be investigated. In this study, we chemically induced hepatic fibrosis in mice using carbon tetrachloride (CCl4) for 6 weeks, which was followed by treatment with a survivin suppressant (YM155). We also evaluated survivin expression in fibrotic human liver tissues, primary HSCs, and HSC cell line by histological analysis. αSMA<sup>+</sup> HSCs in human and mice fibrotic liver tissues showed enhanced survivin expression, whereas the hepatocytes and quiescent (qHSCs) displayed minimal expression. Alternatively, activated M2 macrophage subtype induced survivin expression in HSCs through the TGF-β-TGF-β receptor-I/II signaling. Inhibition of survivin in HSCs promoted cell cycle arrest and senescence, which eventually suppressed their activation. In vivo, YM155 treatment increased the expression of cell senescence makers in HSCs around fibrotic septa such as p53, p21, and <i>β</i>-galactosidase. YM155 treatment in vivo also reduced the hepatic macrophage population and inflammatory cytokine expression in the liver. In conclusion, downregulation of survivin in the fibrotic liver decreases HSC activation by inducing cellular senescence and modulating macrophage cytokine expression that collectively ameliorates liver fibrosis.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2024-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.12015","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139595992","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

Proteome-wide assessment of human interactome as a source of capturing domain–motif and domain-domain interactions 作为捕捉结构域-结构域和结构域-结构域相互作用的来源，对人类相互作用组进行全蛋白质组评估

IF 4.1 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2024-01-19 DOI: 10.1002/ccs3.12014

Sobia Idrees, Keshav Raj Paudel

{"title":"Proteome-wide assessment of human interactome as a source of capturing domain–motif and domain-domain interactions","authors":"Sobia Idrees, Keshav Raj Paudel","doi":"10.1002/ccs3.12014","DOIUrl":"10.1002/ccs3.12014","url":null,"abstract":"<p>Protein–protein interactions (PPIs) play a crucial role in various biological processes by establishing domain–motif (DMI) and domain–domain interactions (DDIs). While the existence of real DMIs/DDIs is generally assumed, it is rarely tested; therefore, this study extensively compared high-throughput methods and public PPI repositories as sources for DMI and DDI prediction based on the assumption that the human interactome provides sufficient data for the reliable identification of DMIs and DDIs. Different datasets from leading high-throughput methods (Yeast two-hybrid [Y2H], Affinity Purification coupled Mass Spectrometry [AP-MS], and Co-fractionation-coupled Mass Spectrometry) were assessed for their ability to capture DMIs and DDIs using known DMI/DDI information. High-throughput methods were not notably worse than PPI databases and, in some cases, appeared better. In conclusion, all PPI datasets demonstrated significant enrichment in DMIs and DDIs (<i>p</i>-value <0.001), establishing Y2H and AP-MS as reliable methods for predicting these interactions. This study provides valuable insights for biologists in selecting appropriate methods for predicting DMIs, ultimately aiding in SLiM discovery.</p>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"18 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2024-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.12014","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139525496","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

Farewell Springer… Hello Wiley 再见了，施普林格，你好，威利:学术科学期刊的故事——“20年后”，《细胞通讯与信号杂志》。

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2023-12-01 DOI: 10.1007/s12079-023-00796-1

Bernard Perbal

引用次数: 0

Use and application of organ-on-a-chip platforms in cancer research 器官芯片平台在癌症研究中的使用与应用。

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2023-11-30 DOI: 10.1007/s12079-023-00790-7

Yifan Yu, TingTing Zhou, Liu Cao

{"title":"Use and application of organ-on-a-chip platforms in cancer research","authors":"Yifan Yu, TingTing Zhou, Liu Cao","doi":"10.1007/s12079-023-00790-7","DOIUrl":"10.1007/s12079-023-00790-7","url":null,"abstract":"<div>\u0000 \u0000 <p>Tumors are a major cause of death worldwide, and much effort has been made to develop appropriate anti-tumor therapies. Existing in vitro and in vivo tumor models cannot reflect the critical features of cancer. The development of organ-on-a-chip models has enabled the integration of organoids, microfluidics, tissue engineering, biomaterials research, and microfabrication, offering conditions that mimic tumor physiology. Three-dimensional in vitro human tumor models that have been established as organ-on-a-chip models contain multiple cell types and a structure that is similar to the primary tumor. These models can be applied to various foci of oncology research. Moreover, the high-throughput features of microfluidic organ-on-a-chip models offer new opportunities for achieving large-scale drug screening and developing more personalized treatments. In this review of the literature, we explore the development of organ-on-a-chip technology and discuss its use as an innovative tool in basic and clinical applications and summarize its advancement of cancer research.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1163-1179"},"PeriodicalIF":3.6,"publicationDate":"2023-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713514/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138460126","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

miRNAs as short non-coding RNAs in regulating doxorubicin resistance mirna作为短链非编码rna调控阿霉素耐药。

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2023-11-29 DOI: 10.1007/s12079-023-00789-0

Sepideh Mirzaei, Mahshid Deldar Abad Paskeh, Farhad Adhami Moghadam, Maliheh Entezari, Zeinab Khazaei Koohpar, Elahe Sadat Hejazi, Shamin Rezaei, Amirabbas Kakavand, Maryam Aboutalebi, Mohammad Arad Zandieh, Romina Rajabi, Shokooh Salimimoghadam, Afshin Taheriazam, Mehrdad Hashemi, Saeed Samarghandian

{"title":"miRNAs as short non-coding RNAs in regulating doxorubicin resistance","authors":"Sepideh Mirzaei, Mahshid Deldar Abad Paskeh, Farhad Adhami Moghadam, Maliheh Entezari, Zeinab Khazaei Koohpar, Elahe Sadat Hejazi, Shamin Rezaei, Amirabbas Kakavand, Maryam Aboutalebi, Mohammad Arad Zandieh, Romina Rajabi, Shokooh Salimimoghadam, Afshin Taheriazam, Mehrdad Hashemi, Saeed Samarghandian","doi":"10.1007/s12079-023-00789-0","DOIUrl":"10.1007/s12079-023-00789-0","url":null,"abstract":"<div>\u0000 \u0000 <p>The treatment of cancer patients has been prohibited by chemoresistance. Doxorubicin (DOX) is an anti-tumor compound disrupting proliferation and triggering cell cycle arrest via inhibiting activity of topoisomerase I and II. miRNAs are endogenous RNAs localized in cytoplasm to reduce gene level. Abnormal expression of miRNAs changes DOX cytotoxicity. Overexpression of tumor-promoting miRNAs induces DOX resistance, while tumor-suppressor miRNAs inhibit DOX resistance. The miRNA-mediated regulation of cell death and hallmarks of cancer can affect response to DOX chemotherapy in tumor cells. The transporters such as P-glycoprotein are regulated by miRNAs in DOX chemotherapy. Upstream mediators including lncRNAs and circRNAs target miRNAs in affecting capacity of DOX. The response to DOX chemotherapy can be facilitated after administration of agents that are mostly phytochemicals including curcumol, honokiol and ursolic acid. These agents can regulate miRNA expression increasing DOX's cytotoxicity. Since delivery of DOX alone or in combination with other drugs and genes can cause synergistic impact, the nanoparticles have been introduced for drug sensitivity.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1181-1202"},"PeriodicalIF":3.6,"publicationDate":"2023-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713513/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138451496","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

Protease-activated receptor 2 attenuates doxorubicin-induced apoptosis in colon cancer cells 蛋白酶激活受体2减弱阿霉素诱导的结肠癌细胞凋亡。

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2023-11-22 DOI: 10.1007/s12079-023-00791-6

Himani Shah, Timothy A. Hill, Junxian Lim, David P. Fairlie

{"title":"Protease-activated receptor 2 attenuates doxorubicin-induced apoptosis in colon cancer cells","authors":"Himani Shah, Timothy A. Hill, Junxian Lim, David P. Fairlie","doi":"10.1007/s12079-023-00791-6","DOIUrl":"10.1007/s12079-023-00791-6","url":null,"abstract":"<div>\u0000 \u0000 <p>Drug resistance represents a major problem in cancer treatment. Doxorubicin (adriamycin) is an injectable DNA intercalating drug that halts cancer cell growth by inhibiting topoisomerase 2, but its long-term effectiveness is compromised by onset of resistance. This study demonstrates that expression of the PAR2 gene in human colon adenocarcinoma tissue samples was the highest among 32 different cancer types (n = 10,989), and higher in colon adenocarcinoma tissues (n = 331) than normal colon tissues (n = 308), revealing an association between PAR2 expression and human colon cancer. HT29 cells are a human colorectal adenocarcinoma cell line that is sensitive to the chemotherapeutic drug doxorubicin and also expresses PAR2. We find that PAR2 activation in HT29 cells, either by an endogenous protease agonist (trypsin) or an exogenous peptide agonist (2f-LIGRL-NH<sub>2</sub>), significantly reduces doxorubicin-induced cell death, reactive oxygen species production, caspase 3/7 activity and cleavage of caspase-8 and caspase-3. Moreover, PAR2-mediated MEK1/2-ERK1/2 pathway induced by 2f-LIGRL-NH<sub>2</sub> leads to upregulated anti-apoptotic MCL-1 and Bcl-xL proteins that promote cellular survival. These findings suggest that activation of PAR2 compromises efficacy of doxorubicin in colon cancer. Further support for this conclusion came from experiments with human colon cancer HT29 cells, either with the PAR2 gene deleted or in the presence of a pharmacological antagonist of PAR2, which showed full restoration of all doxorubicin-mediated effects. Together, these findings reveal a strong link between PAR2 activation and signalling in human colon cancer cells and increased survival against doxorubicin-induced cell death. They support PAR2 antagonism as a possible new strategy for enhancing doxorubicin therapy.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1293-1307"},"PeriodicalIF":3.6,"publicationDate":"2023-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713943/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138291007","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