Hereditas最新文献

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Combination of arsenic trioxide and apatinib synergistically inhibits small cell lung cancer by down-regulating VEGFR2/mTOR and Akt/c-Myc signaling pathway via GRB10. 三氧化二砷和阿帕替尼通过 GRB10 下调 VEGFR2/mTOR 和 Akt/c-Myc 信号通路,从而协同抑制小细胞肺癌。
IF 2.7 3区 生物学
Hereditas Pub Date : 2024-09-02 DOI: 10.1186/s41065-024-00330-2
Yao Yu, Yu Shang, Si Shi, Yaowu He, Wenchao Shi, Menghan Wang, Qi Wang, Dandan Xu, Ce Shi, Hong Chen
{"title":"Combination of arsenic trioxide and apatinib synergistically inhibits small cell lung cancer by down-regulating VEGFR2/mTOR and Akt/c-Myc signaling pathway via GRB10.","authors":"Yao Yu, Yu Shang, Si Shi, Yaowu He, Wenchao Shi, Menghan Wang, Qi Wang, Dandan Xu, Ce Shi, Hong Chen","doi":"10.1186/s41065-024-00330-2","DOIUrl":"10.1186/s41065-024-00330-2","url":null,"abstract":"<p><strong>Background: </strong>Small cell lung carcinoma (SCLC) is characterized by -poor prognosis, -high predilection for -metastasis, -proliferation, and -absence of newer therapeutic options. Elucidation of newer pathways characterizing the disease may allow for development of targeted therapies and consequently favorable outcomes.</p><p><strong>Methods: </strong>The current study explored the combinatorial action of arsenic trioxide (ATO) and apatinib (APA) in vitro and in vivo. In vitro models were tested using -H446 and -H196 SCLC cell lines. The ability of drugs to reduce -metastasis, -cell proliferation, and -migration were assessed. Using bioinformatic analysis, differentially expressed genes were determined. Gene regulation was assessed using gene knock down models and confirmed using Western blots. The in vivo models were used to confirm the resolution of pathognomic features in the presence of the drugs. Growth factor receptor bound protein (GRB) 10 expression levels of human small cell lung cancer tissues and adjacent tissues were detected by IHC.</p><p><strong>Results: </strong>In combination, ATO and APA were found to significantly reduce -cell proliferation, -migration, and -metastasis in both the cell lines. Cell proliferation was found to be inhibited by activation of Caspase-3, -7 pathway. In the presence of drugs, it was found that expression of GRB10 was stabilized. The silencing of GRB10 was found to negatively regulate the VEGFR2/Akt/mTOR and Akt/GSK-3β/c-Myc signaling pathway. Concurrently, absence of metastasis and reduction of tumor volume were confirmed in vivo. The immunohistochemical results confirmed that the expression level of GRB10 in adjacent tissues was significantly higher than that in human small cell lung cancer tissues.</p><p><strong>Conclusions: </strong>Synergistically, ATO and APA have a more significant impact on inhibiting cell proliferation than each drug independently. ATO and APA may be mediating its action through the stabilization of GRB10 thus acting as a tumor suppressor. We thus, preliminarily report the impact of GRB10 stability as a target for SCLC treatment.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11367874/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142119544","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
Correlation between gut microbiota characteristics and non-small cell lung cancer based on macrogenomics sequencing. 基于宏基因组学测序的肠道微生物群特征与非小细胞肺癌之间的相关性。
IF 2.7 3区 生物学
Hereditas Pub Date : 2024-08-27 DOI: 10.1186/s41065-024-00328-w
GuiLin Zeng, LiRong Zeng, Ying Wang, Zhi Cao, XiangHua Zeng, ZhiHong Xue, ShiLan Liu, YaMao Li, Lang He
{"title":"Correlation between gut microbiota characteristics and non-small cell lung cancer based on macrogenomics sequencing.","authors":"GuiLin Zeng, LiRong Zeng, Ying Wang, Zhi Cao, XiangHua Zeng, ZhiHong Xue, ShiLan Liu, YaMao Li, Lang He","doi":"10.1186/s41065-024-00328-w","DOIUrl":"10.1186/s41065-024-00328-w","url":null,"abstract":"<p><strong>Objective: </strong>Non-small cell lung cancer (NSCLC) patients undergoing chemotherapy and immunotherapy experience disturbances in the gut microbiota. This study intends to find out the correlation between gut microbiota and clinical indices before and after radiotherapy for NSCLC.</p><p><strong>Methods: </strong>Ten patients with primary NSCLC were screened, and plasma and fecal samples were collected before and after radiotherapy, respectively. Inflammatory indices in plasma were detected. Genomic DNA was extracted from fecal specimens and sequenced on on Illumina HiSeq2000 sequencing platform. Thee sequenced data were subjected to Metagenome assembly, gene prediction, species annotation, and gene function analysis to study and analyze gut microbiota and metabolic functions. The correlation between the diversity of gut microbiota and the clinical indicators of NSCLC patients was evaluated, and the changes of gut microbiota before and after radiotherapy were observed.</p><p><strong>Results: </strong>The diversity of gut microbiota in NSCLC patients did not correlate with smoking, pathology, and inflammatory markers. The abundance of phylum (p)_Bacteroidetes increased; p_Firmicutes and p_Bacteroidetes accounted for the highest proportion in NSCLC patients, and the abundance of both was dominantly exchanged after radiotherapy. There was a decrease in genus (g)_Bifidobacterium after radiotherapy in NSCLC patients. There was no significant correlation between the diversity of gut microbiota after radiotherapy and radiotherapy sensitivity, and the structural composition and abundance of gut microbiota remained stable.</p><p><strong>Conclusion: </strong>The diversity of gut microbiota is altered after radiotherapy in NSCLC patients, showing an increase in harmful bacteria and a decrease in beneficial bacteria.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11348753/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142080097","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
The novel circFKBP8/miR-432-5p/E2F7 cascade functions as a regulatory network in breast cancer. 新型 circFKBP8/miR-432-5p/E2F7 级联在乳腺癌中发挥着调控网络的作用。
IF 2.7 3区 生物学
Hereditas Pub Date : 2024-08-27 DOI: 10.1186/s41065-024-00331-1
Zhongkui Jin, Wang Xu, Kunlin Yu, Cailu Luo, Xiaodan Luo, Tao Lian, Changshan Liu
{"title":"The novel circFKBP8/miR-432-5p/E2F7 cascade functions as a regulatory network in breast cancer.","authors":"Zhongkui Jin, Wang Xu, Kunlin Yu, Cailu Luo, Xiaodan Luo, Tao Lian, Changshan Liu","doi":"10.1186/s41065-024-00331-1","DOIUrl":"10.1186/s41065-024-00331-1","url":null,"abstract":"<p><strong>Background: </strong>Circular RNAs (circRNAs) are capable of affecting breast cancer (BC) development. However, the role and underneath mechanism of circFKBP8 (also known as hsa_circ_0000915) in BC remain largely unknown.</p><p><strong>Methods: </strong>Expression analyses were performed using quantitative real-time polymerase chain reaction (qRT-PCR), western blot, and immunohistochemistry (IHC) assays. Effects on cell functional phenotypes were determined by assessing cell proliferation, migratory capacity, invasion, and stemness in vitro. The relationship between microRNA (miR)-432-5p and circFKBP8 or E2F transcription factor 7 (E2F7) was examined by RNA pull-down, dual-luciferase reporter, and RNA immunoprecipitation (RIP) assays. Xenograft assays were used to identify the function of circFKBP8 in vivo.</p><p><strong>Results: </strong>CircFKBP8 was presented at high levels in BC tissues and cells. High circFKBP8 expression was associated with worse overall survival in BC patients. CircFKBP8 suppression inhibited BC cell proliferation, migratory capacity, invasion and stemness in vitro. CircFKBP8 suppression blocked xenograft tumor growth in vivo. Mechanistically, circFKBP8 functioned as a miR-432-5p sponge to modulate E2F7 expression. CircFKBP8 modulated BC cell malignant behaviors by miR-432-5p, and miR-432-5p affected these cell phenotypes through E2F7.</p><p><strong>Conclusion: </strong>Our observations prove that circFKBP8 promotes BC malignant phenotypes through the miR-432-5p/E2F7 cascade, offering a promising therapeutic and prognostic target for BC.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11348600/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142080098","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
SOLAMEN syndrome with cardiovascular damage. 伴有心血管损伤的 SOLAMEN 综合征。
IF 2.7 3区 生物学
Hereditas Pub Date : 2024-07-30 DOI: 10.1186/s41065-024-00314-2
Xiong Zhao, Xiaojie Yue, Shifan Yuan, Yefeng Dai, Hao Gu
{"title":"SOLAMEN syndrome with cardiovascular damage.","authors":"Xiong Zhao, Xiaojie Yue, Shifan Yuan, Yefeng Dai, Hao Gu","doi":"10.1186/s41065-024-00314-2","DOIUrl":"10.1186/s41065-024-00314-2","url":null,"abstract":"<p><p>SOLAMEN syndrome is a rare, recently recognized congenital syndrome that is characterized by progressive and hypertrophic diseases involving multiple systems, including segmental overgrowth, lipomatosis, arteriovenous malformation (AVM) and epidermal nevus. According to literatures, SOLAMEN syndrome is caused by heterozygous PTEN mutation. Phenotypic overlap complicates the clinical identification of diseases associated with PTEN heterozygous mutations, making the diagnosis of SOLAMEN more challenging. In addition, SOLAMEN often presents with segmental tissue overgrowth and vascular malformations, increasing the possibility of misdiagnosis as klipple-trenaunay syndrome or Parks-Weber syndrome. Here, we present a case of a child presenting with macrocephaly, patchy lymphatic malformation on the right chest, marked subcutaneous varicosities and capillaries involving the whole body, overgrowth of the left lower limb, a liner epidermal nevus on the middle of the right lower limb, and a large AVM on the right cranial thoracic entrance. Based on the typical phenotypes, the child was diagnosed as SOLAMEN syndrome. detailed clinical, imaging and genetic diagnoses of SOLAMEN syndrome was rendered. Next-generation sequencing (NGS) data revealed that except for a germline PTEN mutation, a PDGFRB variant was also identified. A subsequent echocardiographic examination detected potential cardiac defects. We suggested that given the progressive nature of AVM and the potential severity of cardiac damage, regular echocardiographic evaluation, imaging follow-up and appropriate interventional therapy for AVM are recommended.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2024-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11287979/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141855365","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
Novel Antennapedia and Ultrabithorax trimeric complexes with TBP and Exd regulate transcription. 与 TBP 和 Exd 组成的新型 Antennapedia 和 Ultrabithorax 三聚体复合物可调控转录。
IF 2.7 3区 生物学
Hereditas Pub Date : 2024-07-30 DOI: 10.1186/s41065-024-00327-x
Alely Villarreal-Puente, Claudia Altamirano-Torres, Gustavo Jiménez-Mejía, Carolina Hernández-Bautista, Rubén Montalvo-Méndez, Martha Vázquez, Mario Zurita, Diana Reséndez-Pérez
{"title":"Novel Antennapedia and Ultrabithorax trimeric complexes with TBP and Exd regulate transcription.","authors":"Alely Villarreal-Puente, Claudia Altamirano-Torres, Gustavo Jiménez-Mejía, Carolina Hernández-Bautista, Rubén Montalvo-Méndez, Martha Vázquez, Mario Zurita, Diana Reséndez-Pérez","doi":"10.1186/s41065-024-00327-x","DOIUrl":"10.1186/s41065-024-00327-x","url":null,"abstract":"<p><strong>Background: </strong>Hox proteins interact with DNA and many other proteins, co-factors, transcriptional factors, chromatin remodeling components, non-coding RNAs and even the extracellular matrix that assembles the Hox complexes. The number of interacting partners continues to grow with diverse components and more transcriptional factors than initially thought. Hox complexes present many activities, but their molecular mechanisms to modulate their target genes remain unsolved.</p><p><strong>Results: </strong>In this paper we showed the protein-protein interaction of Antp with Ubx through the homeodomain using BiFC in Drosophila. Analysis of Antp-deletional mutants showed that AntpHD helixes 1 and 2 are required for the interaction with Ubx. Also, we found a novel interaction of Ubx with TBP, in which the PolyQ domain of TBP is required for the interaction. Moreover, we also detected the formation of two new trimeric complexes of Antp with Ubx, TBP and Exd using BiFC-FRET; these proteins, however, do not form a trimeric interaction with BIP2 or TFIIEβ. The novel trimeric complexes reduced Antp transcriptional activity, indicating that they could confer specificity for repression.</p><p><strong>Conclusions: </strong>Our results increase the number of transcriptional factors in the Antp and Ubx interactomes that form two novel trimeric complexes with TBP and Exd. We also report a new Ubx interaction with TBP. These novel interactions provide important clues of the dynamics of Hox-interacting complexes involved in transcriptional regulation, contributing to better understand Hox function.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2024-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11290222/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141855364","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
Correction: Development of a prognostic risk model of uveal melanoma based on N7-methylguanosine-related regulators. 更正:基于 N7-甲基鸟苷相关调节因子的葡萄膜黑色素瘤预后风险模型的开发。
IF 2.7 3区 生物学
Hereditas Pub Date : 2024-07-24 DOI: 10.1186/s41065-024-00326-y
Pingfan Wu, Qian Zhang, Peng Zhong, Li Chai, Qiong Luo, Chengyou Jia
{"title":"Correction: Development of a prognostic risk model of uveal melanoma based on N7-methylguanosine-related regulators.","authors":"Pingfan Wu, Qian Zhang, Peng Zhong, Li Chai, Qiong Luo, Chengyou Jia","doi":"10.1186/s41065-024-00326-y","DOIUrl":"10.1186/s41065-024-00326-y","url":null,"abstract":"","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2024-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11267662/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141758275","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
Development of a prognostic risk model of uveal melanoma based on N7-methylguanosine-related regulators 基于 N7-甲基鸟苷相关调节因子开发葡萄膜黑色素瘤预后风险模型
IF 2.7 3区 生物学
Hereditas Pub Date : 2024-07-10 DOI: 10.1186/s41065-024-00324-0
Pingfan Wu, Qian Zhang, Peng Zhong, Li Chai, Qiong Luo, Chengyou Jia
{"title":"Development of a prognostic risk model of uveal melanoma based on N7-methylguanosine-related regulators","authors":"Pingfan Wu, Qian Zhang, Peng Zhong, Li Chai, Qiong Luo, Chengyou Jia","doi":"10.1186/s41065-024-00324-0","DOIUrl":"https://doi.org/10.1186/s41065-024-00324-0","url":null,"abstract":"Uveal melanoma (UVM) stands as the predominant type of primary intraocular malignancy among adults. The clinical significance of N7-methylguanosine (m7G), a prevalent RNA modifications, in UVM remains unclear. Primary information from 80 UVM patients were analyzed as the training set, incorporating clinical information, mutation annotations and mRNA expression obtained from The Cancer Genome Atlas (TCGA) website. The validation set was carried out using Gene Expression Omnibus (GEO) database GSE22138 and GSE84976. Kaplan–Meier and Cox regression of univariate analyses were subjected to identify m7G-related regulators as prognostic genes. A prognostic risk model comprising EIF4E2, NUDT16, SNUPN and WDR4 was established through Cox regression of LASSO. Evaluation of the model’s predictability for UVM patients’ prognosis by Receiver Operating Characteristic (ROC) curves in the training set, demonstrated excellent performance Area Under the Curve (AUC) > 0.75. The high-risk prognosis within the TCGA cohort exhibit a notable worse outcome. Additionally, an independent correlation between the risk score and overall survival (OS) among UVM patients were identified. External validation of this model was carried out using the validation sets (GSE22138 and GSE84976). Immune-related analysis revealed that patients with high score of m7G-related risk model exhibited elevated level of immune infiltration and immune checkpoint gene expression. We have developed a risk prediction model based on four m7G-related regulators, facilitating effective estimate UVM patients’ survival by clinicians. Our findings shed novel light on essential role of m7G-related regulators in UVM and suggest potential novel targets for the diagnosis, prognosis and therapy of UVM.","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2024-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141573794","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
Knockdown of AMIGO2 suppresses proliferation and migration through regulating PPAR-γ in bladder cancer. 敲除 AMIGO2 可通过调节 PPAR-γ 抑制膀胱癌的增殖和迁移。
IF 2.7 3区 生物学
Hereditas Pub Date : 2024-07-08 DOI: 10.1186/s41065-024-00325-z
Dali Han, Bin Xiong, Xiangxiang Zhang, Chaohu Chen, Zhiqiang Yao, Hao Wu, Jinlong Cao, Jianpeng Li, Pan Li, Zhiping Wang, Junqiang Tian
{"title":"Knockdown of AMIGO2 suppresses proliferation and migration through regulating PPAR-γ in bladder cancer.","authors":"Dali Han, Bin Xiong, Xiangxiang Zhang, Chaohu Chen, Zhiqiang Yao, Hao Wu, Jinlong Cao, Jianpeng Li, Pan Li, Zhiping Wang, Junqiang Tian","doi":"10.1186/s41065-024-00325-z","DOIUrl":"10.1186/s41065-024-00325-z","url":null,"abstract":"<p><strong>Purpose: </strong>This study aims to reveal the relationship between AMIGO2 and proliferation, migration and tumorigenicity of bladder cancer, and explore the potential molecular mechanisms.</p><p><strong>Methods: </strong>The expression level of AMIGO2 is measured by qRT-PCR and immunohistochemistry (IHC). Stable AMIGO2 knockdown cell lines T24 and 5637 were established by lentivirus transfection. Cell Counting Kit (CCK-8 assay) was produced to determine cell proliferation, flow cytometry analysis was utilized to detect cell cycle, and wound healing assay was proceeded to test migration ability of bladder cancer cells. Xenograft mouse model was established for investigating the effect of AMIGO2 on tumor formation in vivo. The RNA Sequencing technology was applied to explore the underlying mechanisms. The expression level of PPAR-γ was measured by Western Blot.</p><p><strong>Results: </strong>AMIGO2 was upregulated in bladder cancer cells and tissues. Inhibited expression of AMIGO2 suppresses cell proliferation and migration. Low AMIGO2 expression inhibited tumorigenicity of 5637 in nude mice. According to RNA-Seq and bioinformatics analysis, 917 DEGs were identified. The DEGs were mainly enriched in cell-cell adhesion, peroxisome proliferators-activated receptors (PPARs) signaling pathway and some other pathways. PPAR-γ is highly expressed in bladder cancer cell lines T24 and 5637, but when AMIGO2 is knocked down in T24 and 5637, the expression level of PPAR-γ is also decreased, and overexpression of PPAR-γ could reverse the suppression effect of cell proliferation and migration caused by the inhibition of AMIGO2.</p><p><strong>Conclusion: </strong>AMIGO2 is overexpressed in bladder cancer cells and tissues. Knockdown of AMIGO2 suppresses bladder cancer cell proliferation and migration. These processes might be regulated by PPAR-γ signaling pathway.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2024-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11229346/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141558648","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
METTL14 contributes to the progression of nasopharyngeal carcinoma through regulating the stability of AOC1 mRNA. METTL14 通过调节 AOC1 mRNA 的稳定性,促进鼻咽癌的进展。
IF 2.7 3区 生物学
Hereditas Pub Date : 2024-07-02 DOI: 10.1186/s41065-024-00317-z
Changan Hu, Shengguan Song, Shanglong Zhao, Zhen Xue, Xiwen Zhu
{"title":"METTL14 contributes to the progression of nasopharyngeal carcinoma through regulating the stability of AOC1 mRNA.","authors":"Changan Hu, Shengguan Song, Shanglong Zhao, Zhen Xue, Xiwen Zhu","doi":"10.1186/s41065-024-00317-z","DOIUrl":"10.1186/s41065-024-00317-z","url":null,"abstract":"<p><strong>Background: </strong>Nasopharyngeal carcinoma (NPC) is a malignant epithelial tumor of the nasopharyngeal mucosa with a high incidence rate all over the world. Methyltransferase-like 14 (METTL14) is a major RNA N6-adenosine methyltransferase implicated in tumor progression by regulating RNA function. This study is designed to explore the biological function and mechanism of METTL14 in NPC.</p><p><strong>Methods: </strong>METTL14 and Amine oxidase copper containing 1 (AOC1) expression were detected by real-time quantitative polymerase chain reaction (RT-qPCR). The protein levels of METTL14, AOC1, Cyclin D1, B-cell lymphoma-2 (Bcl-2), and N-cadherin were measured using western blot. Cell proliferation, cycle progression, apoptosis, migration, and invasion were assessed using 5-ethynyl-2'-deoxyuridine (EdU), Colony formation, flow cytometry, wound scratch, and transwell assays. The interaction between METTL14 and AOC1 was verified using RNA immunoprecipitation (RIP), methylated RNA immunoprecipitation (MeRIP), and dual-luciferase reporter assays. The biological role of METTL14 on NPC tumor growth was examined by the xenograft tumor model in vivo.</p><p><strong>Results: </strong>METTL14 and AOC1 were highly expressed in NPC tissues and cells. Moreover, METTL14 knockdown might block NPC cell proliferation, migration, invasion, and induce cell apoptosis in vitro. In mechanism, METTL14 might enhance the stability of AOC1 mRNA via m6A methylation. METTL14 silencing might repress NPC tumor growth in vivo.</p><p><strong>Conclusion: </strong>METTL14 might boosted the development of NPC cells partly by regulating the stability of AOC1 mRNA, which provided a promising therapeutic target for NPC treatment.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":null,"pages":null},"PeriodicalIF":2.7,"publicationDate":"2024-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11221105/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141491719","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
Comparative chloroplast-specific SNP and nSCoT markers analysis and population structure study in kiwifruit plants. 猕猴桃植物叶绿体特异性 SNP 和 nSCoT 标记比较分析及种群结构研究。
IF 2.7 3区 生物学
Hereditas Pub Date : 2024-05-17 DOI: 10.1186/s41065-024-00321-3
Yinling Ding, Yu Wang, Zhe Chen, Jiamin Dou, Yihao Zhang, Yu Zhang
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