Human Cell最新文献_第8页

Impaired Fanconi anemia pathway causes DNA hypomethylation in human angiosarcomas. 范可尼贫血途径受损导致人血管肉瘤DNA低甲基化。

IF 2.8 3区生物学

Human Cell Pub Date : 2022-09-01 Epub Date: 2022-07-11 DOI: 10.1007/s13577-022-00736-y

Kangning Zhu, Suofeng Sun, Fengxia Guo, Lan Gao

引用次数: 0

Long non‑coding RNA PART1: dual role in cancer. 长链非编码RNA PART1：在癌症中的双重作用

IF 2.8 3区生物学

Human Cell Pub Date : 2022-09-01 Epub Date: 2022-07-21 DOI: 10.1007/s13577-022-00752-y

Rui Ran, Chao-Yang Gong, Zhi-Qiang Wang, Wen-Ming Zhou, Shun-Bai Zhang, Yong-Qiang Shi, Chun-Wei Ma, Hai-Hong Zhang

{"title":"Long non‑coding RNA PART1: dual role in cancer.","authors":"Rui Ran, Chao-Yang Gong, Zhi-Qiang Wang, Wen-Ming Zhou, Shun-Bai Zhang, Yong-Qiang Shi, Chun-Wei Ma, Hai-Hong Zhang","doi":"10.1007/s13577-022-00752-y","DOIUrl":"10.1007/s13577-022-00752-y","url":null,"abstract":"Increasing evidence has shown that long non-coding RNAs (lncRNAs), which are non-coding endogenous single-stranded RNAs, play an essential role in various physiological and pathological processes through transcriptional interference, post-transcriptional regulation, and epigenetic modification. Moreover, lncRNAs, as oncogenes or tumor suppressor genes, play an important role in the occurrence and development of human cancers. Prostate androgen-regulated transcript 1 (PART1) was initially identified as a carcinogenic lncRNA in prostate adenomas. The upregulated expression of PART1 plays a tumor-promoting role in liver, prostate, lung cancers, and other tumors. In contrast, the expression of PART1 is downregulated in esophageal squamous cell carcinoma, glioma, and other tumors, which may inhibit the tumor. PART1 plays a dual role in cancer and regulates cell proliferation, apoptosis, invasion, and metastasis through a variety of potential mechanisms. These findings suggest that PART1 is a promising tumor biomarker and therapeutic target. This article reviews the biological functions, related mechanisms, and potential clinical significance of PART1 in a variety of human cancers.","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 5","pages":"1364-1374"},"PeriodicalIF":2.8,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40613371","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Long noncoding RNA ZBTB40-IT1 regulates bone mass by directing the differentiation of human bone marrow mesenchymal stromal cells via the microRNA-514a-3p/FOXO4 axis. 长链非编码RNA ZBTB40-IT1通过microRNA-514a-3p/FOXO4轴调控人骨髓间充质间质细胞的分化，从而调控骨量

IF 2.8 3区生物学

Human Cell Pub Date : 2022-09-01 Epub Date: 2022-06-09 DOI: 10.1007/s13577-022-00730-4

Zhe Shi, Qiang Zhong, Yuhang Chen, Xin Luo

{"title":"Long noncoding RNA ZBTB40-IT1 regulates bone mass by directing the differentiation of human bone marrow mesenchymal stromal cells via the microRNA-514a-3p/FOXO4 axis.","authors":"Zhe Shi, Qiang Zhong, Yuhang Chen, Xin Luo","doi":"10.1007/s13577-022-00730-4","DOIUrl":"10.1007/s13577-022-00730-4","url":null,"abstract":"This study intended to clarify the mechanism of long noncoding RNA ZBTB40-IT1 in directing human bone marrow-derived mesenchymal stromal cell (hBMSC) differentiation. hBMSCs underwent osteogenic and adipogenic induction, and an osteoporosis mouse model was established via ovariectomy (OVX). Gain- and loss-of-function approaches were utilized in hBMSCs and mice to investigate the function of ZBTB40-IT1, microRNA (miR)-514a-3p, and forkhead box O4 (FOXO4). Dual-luciferase reporter and RNA pulldown assays were applied to evaluate the binding of miR-514a-3p to ZBTB40-IT1 or FOXO4. The femur of the OVX mice had upregulated ZBTB40-IT1 and FOXO4 expression and downregulated miR-514a-3p expression. The bone mass was increased in OVX mice through ZBTB40-IT1 or FOXO4 knockdown. ZBTB40-IT1 and FOXO4 were downregulated, whereas miR-514a-3p was upregulated in osteogenesis-induced hBMSCs, which was the opposite in adipogenesis-induced hBMSCs. ZBTB40-IT1 or FOXO4 knockdown or miR-514a-3p overexpression increased ARS/ALP absorbance and RUNX2 and OCN levels but decreased fat density and PPARγ and FABP4 levels in hBMSCs. Mechanistically, ZBTB40-IT1 elevated FOXO4 expression by binding to miR-514a-3p. miR-514a-3p inhibition annulled the effects of ZBTB40-IT1 downregulation on hBMSC osteogenesis and adipogenesis, and FOXO4 overexpression abolished the impacts of miR-514a-3p upregulation on hBMSC osteogenesis and adipogenesis. Conclusively, ZBTB40-IT1 inhibition promotes the osteogenic differentiation of hBMSCs via the miR-514a-3p/FOXO4 axis, thereby increasing bone mass.","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 1","pages":"1408-1423"},"PeriodicalIF":2.8,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46036308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

ARPC1A is regulated by STAT3 to inhibit ferroptosis and promote prostate cancer progression. ARPC1A受STAT3调控，抑制铁下垂，促进前列腺癌进展。

IF 2.8 3区生物学

Human Cell Pub Date : 2022-09-01 Epub Date: 2022-07-23 DOI: 10.1007/s13577-022-00754-w

Junpeng Ji, Huibing Li, Wenjun Wang, Bo Yuan, Tianyu Shen

{"title":"ARPC1A is regulated by STAT3 to inhibit ferroptosis and promote prostate cancer progression.","authors":"Junpeng Ji, Huibing Li, Wenjun Wang, Bo Yuan, Tianyu Shen","doi":"10.1007/s13577-022-00754-w","DOIUrl":"10.1007/s13577-022-00754-w","url":null,"abstract":"The aim of this study was to investigate the biological function and molecular mechanism of ARPC1A (actin related protein 2/3 complex subunit 1A) in prostate cancer progression. RT-qPCR and IHC results showed that the level of ARPC1A in prostate cancer tissues was significantly higher than that in adjacent tissues. The results of TCGA (the cancer genome atlas) database analysis showed that high expression of ARPC1A indicates poor prognosis in prostate cancer patients. In vitro functional experiments confirmed that downregulation of ARPC1A expression resulted in decreased cell viability and invasive ability of prostate cancer cells, as ARPC1A knockdown promoted ferroptosis. The transcriptional regulation mechanism of STAT3 (signal transduction and activators of transcription 3) on ARPC1A was elucidated by Co-IP, ChIP and luciferase reporter assays. In vivo experiments also supported the in vitro results. We propose that reduced ARPC1A expression inhibits prostate cancer cell viability and invasion in a ferroptotic manner. The ARPC1A level may serve as an independent predictor of prognosis in prostate cancer patients.","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 5","pages":"1591-1601"},"PeriodicalIF":2.8,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40547794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Long non-coding RNA tumor protein 73 antisense RNA 1 influences an interaction between lysine demethylase 5A and promoter of tumor protein 73 to enhance the malignancy of colorectal cancer. 长链非编码RNA肿瘤蛋白73反义RNA 1影响赖氨酸去甲基酶5A与肿瘤蛋白73启动子的相互作用，增强结直肠癌的恶性程度。

IF 2.8 3区生物学

Human Cell Pub Date : 2022-09-01 Epub Date: 2022-07-27 DOI: 10.1007/s13577-022-00740-2

Zhe Huang, He Wang, Mingli Yang

{"title":"Long non-coding RNA tumor protein 73 antisense RNA 1 influences an interaction between lysine demethylase 5A and promoter of tumor protein 73 to enhance the malignancy of colorectal cancer.","authors":"Zhe Huang, He Wang, Mingli Yang","doi":"10.1007/s13577-022-00740-2","DOIUrl":"10.1007/s13577-022-00740-2","url":null,"abstract":"Colorectal cancer (CRC) is one of the leading causes of cancer-related death worldwide. The aim of the present study was to explore the expression level of tumor protein 73 (TP73) in highly malignant CRC tumors and how the long non-coding RNA tumor protein 73 antisense RNA 1 (TP73-AS1) influences that transcription. We found that TP73-AS1 was highly expressed in malignant CRC samples in The Cancer Genome Atlas (TCGA) database. We also demonstrated TP73-AS1 was expressed in thirty samples of CRC tissues collected from China Medical University patients as well as in HCT116, RKO and SW480 CRC cell lines but not in HCoEpiC or CCD-18Co normal colon cells. Only wild-type TP73-AS1, but not any of its alternate splicing isoforms, was positively correlated with tumor malignancy. TP73-AS1 transcripts were shown to be located in cell nuclei especially in close proximity to the TP73 promoter in CRC cells, but not in normal colon cells. In addition, an interaction between lysine demethylase 5A (KDM5A) and TP73-AS1 in CRC cells, but not normal colon cells, and KDM5A localization on the TP73 promoter were influenced by TP73-AS1. Interestingly, the H3K4me3 level on the TP73 promoter was reduced, but was elevated by TP73-AS1 knockdown in CRC cells. In conclusion, these results suggest a novel epigenetic role of TP73-AS1 on histone demethylation that influences TP73 transcription, and shed light on malignancy in CRC.","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 5","pages":"1512-1520"},"PeriodicalIF":2.8,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40649557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Lipocalin-2 inhibits pancreatic cancer stemness via the AKT/c-Jun pathway. 脂联素-2通过AKT/c-Jun通路抑制胰腺癌干性。

IF 2.8 3区生物学

Human Cell Pub Date : 2022-09-01 Epub Date: 2022-07-06 DOI: 10.1007/s13577-022-00735-z

Peipei Hao, Jiamin Zhang, Shu Fang, Miaomiao Jia, Xian Xian, Sinan Yan, Yunpeng Wang, Qian Ren, Fengming Yue, Huixian Cui

{"title":"Lipocalin-2 inhibits pancreatic cancer stemness via the AKT/c-Jun pathway.","authors":"Peipei Hao, Jiamin Zhang, Shu Fang, Miaomiao Jia, Xian Xian, Sinan Yan, Yunpeng Wang, Qian Ren, Fengming Yue, Huixian Cui","doi":"10.1007/s13577-022-00735-z","DOIUrl":"10.1007/s13577-022-00735-z","url":null,"abstract":"Cancer stem cells (CSCs) are involved in cancer recurrence and metastasis owing to their self-renewal properties and drug-resistance capacity. Lipocalin-2 (Lcn2) of the lipocalin superfamily is highly expressed in pancreatic cancer. Nevertheless, reports on the involvement of Lcn2 in the regulation of pancreatic CSC properties are scant. This study is purposed to investigate whether Lcn2 plays a crucial role in CSC renewal and stemness maintenance in pancreatic carcinoma. Immunohistochemistry results of tumor tissue chips together with Gene Expression Omnibus sequencing files confirmed that Lcn2 is highly expressed in pancreatic carcinoma compared with that in normal tissues. The exogenous expression of Lcn2 attenuated CSC-associated SOX2, CD44, and EpCAM expression and suppressed sarcosphere formation and tumorigenesis in the pancreatic carcinoma cell line PANC-1, which showed low expression of Lcn2. However, Lcn2 knockout in BxPC-3 cell line, which presented high Lcn2 expression, promoted CSC stemness, further enhancing sarcosphere formation and tumorigenesis. Moreover, Lcn2 was found to regulate stemness in pancreatic cancer depending on the activation of AKT and c-Jun. Lcn2 suppresses stemness properties in pancreatic carcinoma by activating the AKT-c-Jun pathway, and thus, it may be a novel candidate to suppress the stemness of pancreatic cancer. This study provides a new insight into disease progression.","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 5","pages":"1475-1486"},"PeriodicalIF":2.8,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40566491","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Establishment and characterization of NCC-GCTB5-C1: a novel cell line of giant cell tumor of bone. 骨巨细胞瘤新细胞系NCC-GCTB5-C1的建立与表征

IF 2.8 3区生物学

Human Cell Pub Date : 2022-09-01 Epub Date: 2022-06-02 DOI: 10.1007/s13577-022-00724-2

Taro Akiyama, Yuki Yoshimatsu, Rei Noguchi, Yooksil Sin, Ryuto Tsuchiya, Takuya Ono, Suguru Fukushima, Yu Toda, Naoki Kojima, Akihiko Yoshida, Seji Ohtori, Akira Kawai, Tadashi Kondo

{"title":"Establishment and characterization of NCC-GCTB5-C1: a novel cell line of giant cell tumor of bone.","authors":"Taro Akiyama, Yuki Yoshimatsu, Rei Noguchi, Yooksil Sin, Ryuto Tsuchiya, Takuya Ono, Suguru Fukushima, Yu Toda, Naoki Kojima, Akihiko Yoshida, Seji Ohtori, Akira Kawai, Tadashi Kondo","doi":"10.1007/s13577-022-00724-2","DOIUrl":"10.1007/s13577-022-00724-2","url":null,"abstract":"Giant cell tumor of bone (GCTB), is a rare intermediate malignant bone tumor with high local infiltrative ability, and is genetically characterized by mutation in the H3-3A gene. Standard treatment is curative surgical tumor resection. GCTB demonstrates both local recurrence and pulmonary metastasis after surgical treatment, and effective systematic chemotherapy is yet to be established. Therefore, development of novel chemotherapies for GCTB is necessary. Although patient-derived tumor cell lines are potent tools for preclinical research, 15 GCTB cell lines have been reported to date, and only four are publicly available. Thus, this study aimed to establish and characterize a novel GCTB cell line for preclinical studies on GCTB. Herein, we described the establishment of a cell line, NCC-GCTB5-C1, from the primary tumor tissue of a patient with GCTB. NCC-GCTB5-C1 was shown to harbor a mutation in the H3-3A gene, which is typical of GCTB; thus, it has useful properties for in vitro studies. We conducted the largest integrated screening analysis of 214 antitumor agents using NCC-GCTB5-C1 along with four GCTB cell lines. Romidepsin (a histone deacetylase inhibitor), camptothecin, and actinomycin D (topoisomerase inhibitors) demonstrated remarkable antitumor effects, suggesting that these antitumor agents are potential therapeutic candidates for GCTB treatment. Therefore, the NCC-GCTB5-C1 cell line could potentially contribute to the elucidation of GCTB pathogenesis and the development of novel GCTB treatments.","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 1","pages":"1621-1629"},"PeriodicalIF":2.8,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44015940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

RIG-I acts as a tumor suppressor in melanoma via regulating the activation of the MKK/p38MAPK signaling pathway. RIG-I通过调节MKK/p38MAPK信号通路的激活，在黑色素瘤中发挥肿瘤抑制作用

IF 4.3 3区生物学

Human Cell Pub Date : 2022-07-01 Epub Date: 2022-04-13 DOI: 10.1007/s13577-022-00698-1

Rui Guo, Shun-Yuan Lu, Jin-Xia Ma, Qian-Lan Wang, Lu Zhang, Ling-Yun Tang, Yan Shen, Chun-Ling Shen, Jin-Jin Wang, Li-Ming Lu, Zhu-Gang Wang, Hong-Xin Zhang

{"title":"RIG-I acts as a tumor suppressor in melanoma via regulating the activation of the MKK/p38MAPK signaling pathway.","authors":"Rui Guo, Shun-Yuan Lu, Jin-Xia Ma, Qian-Lan Wang, Lu Zhang, Ling-Yun Tang, Yan Shen, Chun-Ling Shen, Jin-Jin Wang, Li-Ming Lu, Zhu-Gang Wang, Hong-Xin Zhang","doi":"10.1007/s13577-022-00698-1","DOIUrl":"10.1007/s13577-022-00698-1","url":null,"abstract":"Studies have indicated that RIG-I may act as a tumor suppressor and participate in the tumorigenesis of some malignant diseases. However, RIG-I induces distinct cellular responses via different downstream signaling pathways depending on the cell type. To investigate the biological function and underlying molecular mechanism of RIG-I in the tumorigenesis of melanoma, we constructed RIG-I knockout, RIG-I-overexpressing B16-F10 and RIG-I knockdown A375 melanoma cell lines, and analyzed the RIG-I-mediated change in the biological behavior of tumor cells in spontaneous and poly (I:C)-induced RIG-I activation. Cell proliferation, cell cycling, apoptosis and migration were detected by CCK-8 assay, BrdU incorporation assay, Annexin V-PI staining assay and Transwell assay, respectively. In vivo tumorigenicity was evaluated by tumor xenograft growth in nude mice and subsequently by Ki67 staining and TUNEL assays. Furthermore, Western blotting was utilized to explore the underlying mechanism of RIG-I in melanoma cells. Our data showed that RIG-I promotes apoptosis and inhibits proliferation by G1 phase cell cycle arrest in the melanoma cell lines. Mechanistically, RIG-I induced the phosphorylation of p38 MAPK and MAPK kinases MKK3 and MKK4. In conclusion, the current study demonstrated that RIG-I suppressed the development of melanoma by regulating the activity of the MKK/p38 MAPK signaling pathway, which is relevant to research on novel therapeutic targets for this malignant disease.","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 1","pages":"1071-1083"},"PeriodicalIF":4.3,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9226095/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45370864","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: 3

Regulation of osteogenic differentiation by the pro-inflammatory cytokines IL-1β and TNF-α: current conclusions and controversies. 促炎因子IL-1β和TNF-α对成骨分化的调控:目前的结论和争议

IF 2.8 3区生物学

Human Cell Pub Date : 2022-07-01 Epub Date: 2022-05-06 DOI: 10.1007/s13577-022-00711-7

Qingyun Mo, Wei Zhang, Aijing Zhu, Ludvig J Backman, Jialin Chen

引用次数: 0

The α5-nAChR/PD-L1 axis facilitates lung adenocarcinoma cell migration and invasion. α5-nAChR/PD-L1轴促进肺腺癌细胞的迁移和侵袭

IF 2.8 3区生物学

Human Cell Pub Date : 2022-07-01 Epub Date: 2022-05-20 DOI: 10.1007/s13577-022-00709-1

Ping Zhu, Guiyu Kang, Yang Jiao, Chengzhi Gui, Huiping Fan, Xiangying Li, Yanfei Jia, Lulu Zhang, Xiaoli Ma

{"title":"The α5-nAChR/PD-L1 axis facilitates lung adenocarcinoma cell migration and invasion.","authors":"Ping Zhu, Guiyu Kang, Yang Jiao, Chengzhi Gui, Huiping Fan, Xiangying Li, Yanfei Jia, Lulu Zhang, Xiaoli Ma","doi":"10.1007/s13577-022-00709-1","DOIUrl":"10.1007/s13577-022-00709-1","url":null,"abstract":"α5 nicotinic acetylcholine receptor (α5-nAChR) is associated with the progression of smoking-related lung adenocarcinoma (LUAD), but the molecular mechanism is unclear. Programmed death ligand 1 (PD-L1) is encoded by the CD274 gene, which not only inhibits the immune system, but also plays a unique role in tumor growth and metastasis. Here, we gained important insights into the underlying mechanism between α5-nAChR and PD-L1 in LUAD progression. α5-nAChR was overexpressed in various histological subtypes, cancer stages and metastasis statuses of LUAD. The group that coexpressed α5-nAChR and PD-L1 had a worse prognosis than the other subgroups at different stages of LUAD lymph node metastasis. The expression of α5-nAChR and PD-L1 was associated with epithelial-mesenchymal transition (EMT) marker CDH2. In vitro, α5-nAChR mediated nicotine-induced PD-L1 expression via STAT3 and the expression of EMT markers. Downregulation of α5-nAChR and/or PD-L1 inhibited EMT marker expression, cell proliferation, migration and invasion compared to silencing α5-nAChR or PD-L1 alone in LUAD cells. Furthermore, α5-nAChR expression was associated with PD-L1 and EMT marker expression in mouse xenograft models. These results highlight that α5-nAChR mediates STAT3/PD-L1 signaling, which contributes to cell migration and invasion. Therefore, our study may reveal a new interaction between α5-nAChR and PD-L1 that is involved in tumor cell growth and progression in LUAD, which may be a promising target for NSCLC diagnosis and immunotherapy.","PeriodicalId":13228,"journal":{"name":"Human Cell","volume":"35 1","pages":"1207-1218"},"PeriodicalIF":2.8,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45880835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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