Molecular Oncology最新文献_第2页

Retraction statement: Consistency analysis of microRNA‐arm expression reveals microRNA‐369‐5p/3p as tumor suppressors in gastric cancer 撤回声明：微小RNA臂表达的一致性分析显示微小RNA-369-5p/3p是癌症的肿瘤抑制剂

IF 6.6 2区医学

Molecular Oncology Pub Date : 2022-12-01 DOI: 10.1002/1878-0261.13331

Kevin J. Ryan

引用次数: 1

Retraction statement: Down‐regulation of long noncoding RNA PVT1 inhibits esophageal carcinoma cell migration and invasion and promotes cell apoptosis via microRNA‐145‐mediated inhibition of FSCN1 撤回声明：下调长链非编码RNA PVT1通过microRNA-145介导的FSCN1抑制食管癌细胞迁移和侵袭并促进细胞凋亡

IF 6.6 2区医学

Molecular Oncology Pub Date : 2022-12-01 DOI: 10.1002/1878-0261.13332

K. Ryan

引用次数: 0

Issue Information 问题信息

IF 6.6 2区医学

Molecular Oncology Pub Date : 2022-11-26 DOI: 10.1111/ijtd.12229

引用次数: 0

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IF 6.6 2区医学

Molecular Oncology Pub Date : 2022-11-01 DOI: 10.1002/1878-0261.13008

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IF 6.6 2区医学

Molecular Oncology Pub Date : 2022-10-01 DOI: 10.1002/1878-0261.13007

引用次数: 0

Altered splicing of ATG16-L1 mediates acquired resistance to tyrosine kinase inhibitors of EGFR by blocking autophagy in non-small cell lung cancer. ATG16‐L1剪接改变通过阻断非小细胞肺癌的自噬介导对EGFR酪氨酸激酶抑制剂的获得性耐药

IF 4.5 2区医学

Molecular Oncology Pub Date : 2022-10-01 Epub Date: 2022-08-30 DOI: 10.1002/1878-0261.13229

Anne-Sophie Hatat, Clara Benoit-Pilven, Amélie Pucciarelli, Florence de Fraipont, Lucie Lamothe, Pascal Perron, Amandine Rey, Matteo Giaj Levra, Anne-Claire Toffart, Didier Auboeuf, Beatrice Eymin, Sylvie Gazzeri

{"title":"Altered splicing of ATG16-L1 mediates acquired resistance to tyrosine kinase inhibitors of EGFR by blocking autophagy in non-small cell lung cancer.","authors":"Anne-Sophie Hatat, Clara Benoit-Pilven, Amélie Pucciarelli, Florence de Fraipont, Lucie Lamothe, Pascal Perron, Amandine Rey, Matteo Giaj Levra, Anne-Claire Toffart, Didier Auboeuf, Beatrice Eymin, Sylvie Gazzeri","doi":"10.1002/1878-0261.13229","DOIUrl":"10.1002/1878-0261.13229","url":null,"abstract":"Despite the initial efficacy of using tyrosine kinase inhibitors of epidermal growth factor receptors (EGFR-TKIs) for treating patients with non-small cell lung cancer (NSCLC), resistance inevitably develops. Recent studies highlight a link between alternative splicing and cancer drug response. Therefore, we aimed to identify deregulated splicing events that play a role in resistance to EGFR-TKI. By using RNA sequencing, reverse-transcription PCR (RT-PCR), and RNA interference, we showed that overexpression of a splice variant of the autophagic gene ATG16-L1 that retains exon 8 and encodes the β-isoform of autophagy-related protein 16-1 (ATG16-L1 β) concurs acquired resistance to EGFR-TKI in NSCLC cells. Using matched biopsies, we found increased levels of ATG16-L1 β at the time of progression in 3 of 11 NSCLC patients treated with EGFR-TKI. Mechanistically, gefitinib-induced autophagy was impaired in resistant cells that accumulated ATG16-L1 β. Neutralization of ATG16-L1 β restored autophagy in response to gefitinib, induced apoptosis, and inhibited the growth of in ovo tumor xenografts. Conversely, overexpression of ATG16-L1 β in parental sensitive cells prevented gefitinib-induced autophagy and increased cell survival. These results support a role of defective autophagy in acquired resistance to EGFR-TKIs and identify splicing regulation of ATG16-L1 as a therapeutic vulnerability that could be explored for improving EGFR-targeted cancer therapy.","PeriodicalId":51134,"journal":{"name":"Molecular Oncology","volume":"16 1","pages":"3490-3508"},"PeriodicalIF":4.5,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9533692/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41356081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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IF 6.6 2区医学

Molecular Oncology Pub Date : 2022-09-01 DOI: 10.5694/mja2.50641

引用次数: 0

Cellular senescence and the tumour microenvironment. 细胞衰老与肿瘤微环境

IF 5 2区医学

Molecular Oncology Pub Date : 2022-09-01 Epub Date: 2022-06-26 DOI: 10.1002/1878-0261.13268

Masaki Takasugi, Yuya Yoshida, Naoko Ohtani

{"title":"Cellular senescence and the tumour microenvironment.","authors":"Masaki Takasugi, Yuya Yoshida, Naoko Ohtani","doi":"10.1002/1878-0261.13268","DOIUrl":"10.1002/1878-0261.13268","url":null,"abstract":"The senescence-associated secretory phenotype (SASP), where senescent cells produce a variety of secreted proteins including inflammatory cytokines, chemokines, matrix remodelling factors, growth factors and so on, plays pivotal but varying roles in the tumour microenvironment. The effects of SASP on the surrounding microenvironment depend on the cell type and process of cellular senescence induction, which is often associated with innate immunity. Via SASP-mediated paracrine effects, senescent cells can remodel the surrounding tissues by modulating the character of adjacent cells, such as stromal, immune cells, as well as cancer cells. The SASP is associated with both tumour-suppressive and tumour-promoting effects, as observed in senescence surveillance effects (tumour-suppressive) and suppression of anti-tumour immunity in most senescent cancer-associated fibroblasts and senescent T cells (tumour-promoting). In this review, we discuss the features and roles of senescent cells in tumour microenvironment with emphasis on their context-dependency that determines whether they promote or suppress cancer development. Potential usage of recently developed drugs that suppress the SASP (senomorphics) or selectively kill senescence cells (senolytics) in cancer therapy are also discussed.","PeriodicalId":51134,"journal":{"name":"Molecular Oncology","volume":"16 1","pages":"3333-3351"},"PeriodicalIF":5.0,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9490140/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44122643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Autophagy at the intersection of aging, senescence, and cancer. 自噬在衰老、衰老和癌症的交叉点

IF 5 2区医学

Molecular Oncology Pub Date : 2022-09-01 Epub Date: 2022-07-09 DOI: 10.1002/1878-0261.13269

Liam D Cassidy, Masashi Narita

引用次数: 0

USP28 enables oncogenic transformation of respiratory cells, and its inhibition potentiates molecular therapy targeting mutant EGFR, BRAF and PI3K. USP28能够实现呼吸道细胞的致癌转化，其抑制作用增强了针对突变EGFR、BRAF和PI3K的分子治疗

IF 4.5 2区医学

Molecular Oncology Pub Date : 2022-09-01 Epub Date: 2022-04-30 DOI: 10.1002/1878-0261.13217

Cristian Prieto-Garcia, Oliver Hartmann, Michaela Reissland, Fabian Braun, Süleyman Bozkurt, Nikolett Pahor, Carmina Fuss, Andreas Schirbel, Christina Schülein-Völk, Alexander Buchberger, Marco A Calzado Canale, Mathias Rosenfeldt, Ivan Dikic, Christian Münch, Markus E Diefenbacher

{"title":"USP28 enables oncogenic transformation of respiratory cells, and its inhibition potentiates molecular therapy targeting mutant EGFR, BRAF and PI3K.","authors":"Cristian Prieto-Garcia, Oliver Hartmann, Michaela Reissland, Fabian Braun, Süleyman Bozkurt, Nikolett Pahor, Carmina Fuss, Andreas Schirbel, Christina Schülein-Völk, Alexander Buchberger, Marco A Calzado Canale, Mathias Rosenfeldt, Ivan Dikic, Christian Münch, Markus E Diefenbacher","doi":"10.1002/1878-0261.13217","DOIUrl":"10.1002/1878-0261.13217","url":null,"abstract":"Oncogenic transformation of lung epithelial cells is a multistep process, frequently starting with the inactivation of tumour suppressors and subsequent development of activating mutations in proto-oncogenes, such as members of the PI3K or MAPK families. Cells undergoing transformation have to adjust to changes, including altered metabolic requirements. This is achieved, in part, by modulating the protein abundance of transcription factors. Here, we report that the ubiquitin carboxyl-terminal hydrolase 28 (USP28) enables oncogenic reprogramming by regulating the protein abundance of proto-oncogenes such as c-JUN, c-MYC, NOTCH and ∆NP63 at early stages of malignant transformation. USP28 levels are increased in cancer compared with in normal cells due to a feed-forward loop, driven by increased amounts of oncogenic transcription factors such as c-MYC and c-JUN. Irrespective of oncogenic driver, interference with USP28 abundance or activity suppresses growth and survival of transformed lung cells. Furthermore, inhibition of USP28 via a small-molecule inhibitor resets the proteome of transformed cells towards a 'premalignant' state, and its inhibition synergizes with clinically established compounds used to target EGFRL858R -, BRAFV600E - or PI3KH1047R -driven tumour cells. Targeting USP28 protein abundance at an early stage via inhibition of its activity is therefore a feasible strategy for the treatment of early-stage lung tumours, and the observed synergism with current standard-of-care inhibitors holds the potential for improved targeting of established tumours.","PeriodicalId":51134,"journal":{"name":"Molecular Oncology","volume":"16 1","pages":"3082-3106"},"PeriodicalIF":4.5,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9441007/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48037862","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0