Human Cell最新文献_第8页

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 4.3 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":"https://doi.org/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":4.3,"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: 4

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 4.3 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":"https://doi.org/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":4.3,"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: 4

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 4.3 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":"https://doi.org/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":4.3,"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: 1

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 4.3 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":4.3,"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: 1

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

Increased neuropilin-1 expression by COVID-19: a possible cause of long-term neurological complications and progression of primary brain tumors. COVID-19导致神经匹林-1表达增加:可能导致长期神经系统并发症和原发性脑肿瘤进展

IF 4.3 3区生物学

Human Cell Pub Date : 2022-07-01 Epub Date: 2022-05-09 DOI: 10.1007/s13577-022-00716-2

Hamidreza Zalpoor, Hooriyeh Shapourian, Abdullatif Akbari, Shaghayegh Shahveh, Leila Haghshenas

引用次数: 0

miR-203a-3p-DNMT3B feedback loop facilitates non-small cell lung cancer progression. miR-203a-3p-DNMT3B反馈回路促进非小细胞肺癌癌症进展

IF 4.3 3区生物学

Human Cell Pub Date : 2022-07-01 Epub Date: 2022-06-07 DOI: 10.1007/s13577-022-00728-y

Pingshan Yang, Dongdong Zhang, Fengli Zhou, Wenyou Chen, Chuang Hu, Duqing Xiao, Songwang Cai

引用次数: 2

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 4.3 3区生物学

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

Zhe Shi, Qiang Zhong, Yuhang Chen, Xi Luo

引用次数: 2

Long non-coding RNA TRIM52-AS1 sponges microRNA-577 to facilitate diffuse large B cell lymphoma progression via increasing TRIM52 expression 长链非编码RNA TRIM52- as1通过增加TRIM52的表达来抑制microRNA-577促进弥漫性大B细胞淋巴瘤的进展

IF 4.3 3区生物学

Human Cell Pub Date : 2022-06-08 DOI: 10.1007/s13577-022-00725-1

Fang Zhao, Shu-cui Li, Jingjing Liu, Juan Wang, Bo Yang

引用次数: 2

Transcriptomic and epigenomic analyses explore the potential role of H3K4me3 in neomycin-induced cochlear Lgr5+ progenitor cell regeneration of hair cells 转录组学和表观基因组学分析探讨H3K4me3在新霉素诱导的耳蜗Lgr5中的潜在作用+ 毛细胞的祖细胞再生

IF 4.3 3区生物学

Human Cell Pub Date : 2022-06-06 DOI: 10.1007/s13577-022-00727-z

Xiangyu Ma, Shasha Zhang, Shijie Qin, Jiamin Guo, Jia Yuan, Ruiying Qiang, Sha Zhou, Wei Cao, Jianming Yang, Fei Ma, R. Chai

引用次数: 3