{"title":"Retraction statement: Consistency analysis of microRNA‐arm expression reveals microRNA‐369‐5p/3p as tumor suppressors in gastric cancer","authors":"Kevin J. Ryan","doi":"10.1002/1878-0261.13331","DOIUrl":"https://doi.org/10.1002/1878-0261.13331","url":null,"abstract":"The above article, published online on 04 June 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors, the journal Editor in Chief, Kevin Ryan, FEBS Press and John Wiley and Sons Ltd. The retraction has been agreed due to the identification of reuse of images from Figs 3 and 4 in at least six other publications, purporting different experiments. Two of these publications came from the same laboratory, and four from other laboratories. Given the extent of the identified issues, the Editors have decided to retract the article.","PeriodicalId":51134,"journal":{"name":"Molecular Oncology","volume":"16 1","pages":"4060 - 4060"},"PeriodicalIF":6.6,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46598962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"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","authors":"K. Ryan","doi":"10.1002/1878-0261.13332","DOIUrl":"https://doi.org/10.1002/1878-0261.13332","url":null,"abstract":"The above article, published online on 01 August 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Kevin Ryan, FEBS Press, and John Wiley and Sons Ltd. The retraction has been agreed due to observed anomalies in the Western blots on figure 3B and D, the flow cytometry plots in figure 2C, and the wound healing assays in figure 7A and C. The authors were unable to provide compelling raw data underpinning figures 2, 3, 7, and 8.","PeriodicalId":51134,"journal":{"name":"Molecular Oncology","volume":"16 1","pages":"4061 - 4061"},"PeriodicalIF":6.6,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42566755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Molecular OncologyPub Date : 2022-09-01Epub Date: 2022-06-26DOI: 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":"<p><p>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.</p>","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}
Molecular OncologyPub Date : 2022-09-01Epub Date: 2022-07-09DOI: 10.1002/1878-0261.13269
Liam D Cassidy, Masashi Narita
{"title":"Autophagy at the intersection of aging, senescence, and cancer.","authors":"Liam D Cassidy, Masashi Narita","doi":"10.1002/1878-0261.13269","DOIUrl":"10.1002/1878-0261.13269","url":null,"abstract":"<p><p>Autophagy is an evolutionarily conserved cellular process in which macromolecules undergo lysosomal degradation. It fulfills essential roles in quality controlling cellular constituents and in energy homeostasis. Basal autophagy is also widely accepted to provide a protective role in aging and aging-related disorders, and its decline with age might precipitate the onset of a variety of diseases. In this review, we discuss the role of basal autophagy in maintaining homeostasis, in part through the maintenance of stem cell populations and the prevention of cellular senescence. We also consider how stress-induced senescence, for example, during oncogene activation and in premalignant disease, might rely on autophagy, and the possibility that the age-associated decline in autophagy might promote tumour development through a variety of mechanisms. Ultimately, evidence suggests that autophagy is required for malignant cancer progression in a number of settings. Thus, autophagy appears to be tumour-suppressive during the early stages of tumorigenesis and tumour-promoting at later stages.</p>","PeriodicalId":51134,"journal":{"name":"Molecular Oncology","volume":"16 1","pages":"3259-3275"},"PeriodicalIF":5.0,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9490138/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44680069","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}
{"title":"NNK from tobacco smoking enhances pancreatic cancer cell stemness and chemoresistance by creating a β2AR-Akt feedback loop that activates autophagy.","authors":"Xin Chen, Weifan Zhang, Rujuan Liu, Zeen Zhu, Mengyuan Gong, Qiqi Wang, Weikun Qian, Zheng Wu, Qingyong Ma, Zheng Wang","doi":"10.1002/1878-0261.13230","DOIUrl":"10.1002/1878-0261.13230","url":null,"abstract":"<p><p>Low responsiveness to chemotherapy is an important cause of poor prognosis in pancreatic cancer. Smoking is a high-risk factor for pancreatic cancer and cancer resistance to gemcitabine; however, the underlying mechanisms remain unclear. 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is the main metabolite of tobacco burning and has been shown to be associated with cancer development and chemoresistance. However, in pancreatic cancer, its mechanism remains poorly understood. In this study, we found that NNK promoted stemness and gemcitabine resistance in pancreatic cancer cell lines. Moreover, NNK increased autophagy and elevated the expression levels of the autophagy-related markers autophagy-related gene 5 (ATG5), autophagy-related gene 7 (ATG7), and Beclin1. Furthermore, the results showed that NNK-promoted stemness and gemcitabine resistance was partially dependent on the role of NNK in cell autophagy, which is mediated by the β2-adrenergic receptor (β2AR)-Akt axis. Finally, we proved that NNK intervention could not only activate β2AR, but also increase its expression, making β2AR and Akt form a feedback loop. Overall, these findings show that the NNK-induced β2AR-Akt feedback loop promotes stemness and gemcitabine resistance in pancreatic cancer cells.</p>","PeriodicalId":51134,"journal":{"name":"Molecular Oncology","volume":"16 1","pages":"2881-2895"},"PeriodicalIF":6.6,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9348597/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46647794","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}