Cancer Biology

Protein phosphatase 1 regulatory inhibitor subunit 14C promotes triple‐negative breast cancer progression via sustaining inactive glycogen synthase kinase 3 beta

1. Yunting Jian
2. Lingzhi Kong
3. Hongyi Xu
4. Yawei Shi
5. Xinjian Huang
6. Wenjing Zhong
7. Shumei Huang
8. Yue Li
9. Dongni Shi
10. Yunyun Xiao
11. Muwen Yang
12. Siqi Li
13. Xiangfu Chen
14. Ying Ouyang
15. Yameng Hu
16. Xin Chen
17. Libing Song
18. Runyi Ye
19. Weidong Wei

• Curated by eLife

  Evaluation Summary:

  The manuscript presents data that high expression of Protein Phosphatase 1 (PP1) inhibitor in triple-negative breast cancer contributes to poor outcomes by downregulation of an important kinase, GSK3β. The study clearly demonstrates that changes in PPP1R14C expression alter the behaviour of the studied cancer cells and mouse models and proposes a mechanism linking PP1 inhibitor to GSK3β. If this mechanism were substantiated, this would enhance our understanding of the pathophysiology of this important disease and might suggest new treatment options.

  (This preprint has been reviewed by eLife. We include the public reviews from the reviewers here; the authors also receive private feedback with suggested changes to the manuscript. The reviewers remained anonymous to the authors.)

Reviewed by eLife

Comprehensive Analysis of Co-Mutations Identifies Cooperating Mechanisms of Tumorigenesis

1. Limin Jiang
2. Hui Yu
3. Scott Ness
4. Peng Mao
5. Fei Guo
6. Jijun Tang
7. Yan Guo

• Curated by eLife

  Evaluation Summary:

  This paper provides a comprehensive co-mutation analysis of over 30 thousand cancer patients and 1700+ cancer cell lines to identify associations with prognosis and drug resistance that could have translational value for clinical practice. Once validated, it would provide a useful framework for precision oncology.

  “(This preprint has been reviewed by eLife. We include the public reviews from the reviewers here; the authors also receive private feedback with suggested changes to the manuscript.The reviewers remained anonymous to the authors.”.)

Reviewed by eLife

Integrating multi-omics data reveals function and therapeutic potential of deubiquitinating enzymes

1. Laura M Doherty
2. Caitlin E Mills
3. Sarah A Boswell
4. Xiaoxi Liu
5. Charles Tapley Hoyt
6. Benjamin Gyori
7. Sara J Buhrlage
8. Peter K Sorger

• Curated by eLife

  Evaluation Summary:

  To better understand proteins and pathways regulated by deubiquitinating enzymes (DUBs), this study has assembled a database that integrates existing datasets with additional knock-out experiments. Co-dependent genes as well as protein-protein interactions and co-expression were taken into account. The combined data confirms known functions and highlights potential new functions of DUBs. This will be a useful resource for investigators aiming to elucidate DUB functions, as well as for research efforts to develop therapies for the treatment of different cancer types through targeting DUBs.

  (This preprint has been reviewed by eLife. We include the public reviews from the reviewers here; the authors also receive private feedback with suggested changes to the manuscript. Reviewer #3 agreed to share their name with the authors.)

Reviewed by eLife

Solute exchange through gap junctions lessens the adverse effects of inactivating mutations in metabolite-handling genes

1. Stefania Monterisi
2. Johanna Michl
3. Alzbeta Hulikova
4. Jana Koth
5. Esther M Bridges
6. Amaryllis E Hill
7. Gulnar Abdullayeva
8. Walter F Bodmer
9. Pawel Swietach

• Curated by eLife

  Evaluation Summary:

  This work shows that spontaneous mutations in cancer cells affecting metabolic pathways do not necessarily result in functional defects, as affected cells may be able to be rescued by gap junction-mediated exchange of metabolites. This is verified in three specific examples, although some of the "quantitative" methods of measuring gap junctional coupling are actually only qualitative in nature. In addition, more experiments are needed to address the effect of Cx31 and Cx43 KD. This paper is of potential interest to a broad readership in cancer biology as well as colleagues studying metabolic pathways.

  (This preprint has been reviewed by eLife. We include the public reviews from the reviewers here; the authors also receive private feedback with suggested changes to the manuscript. Reviewer #2 agreed to share their name with the authors.)

Reviewed by eLife

The network of SARS-CoV-2—cancer molecular interactions and pathways

1. Pau Erola
2. Richard M. Martin
3. Tom R. Gaunt

Reviewed by ScreenIT

Widespread multi-targeted therapy resistance via drug-induced secretome fucosylation

1. Mark Borris D. Aldonza
2. Junghwa Cha
3. Insung Yong
4. Jayoung Ku
5. Dabin Lee
6. Pavel Sinitcyn
7. Ryeong-Eun Cho
8. Roben D. Delos Reyes
9. Dongwook Kim
10. Hye-Jin Sung
11. Soyeon Kim
12. Minjeong Kang
13. Yongsuk Ku
14. Geonho Park
15. Han Suk Ryu
16. Sukki Cho
17. Tae Min Kim
18. Pilnam Kim
19. Je-Yoel Cho
20. Yoosik Kim

• Curated by eLife

  Evaluation Summary:

  This manuscript provides a comprehensive unbiased analysis of the fucosylation secretome and correlates with drug response in cancer. It uses a combination of bioinformatic based analyses of multiple datasets and cell based data to identify changes in the secretome and correlates this to drug responses to several targeted therapies.

  (This preprint has been reviewed by eLife. We include the public reviews from the reviewers here; the authors also receive private feedback with suggested changes to the manuscript. Reviewer #3 agreed to share their name with the authors.)

Reviewed by eLife

The oncoprotein BCL6 enables solid tumor cells to evade genotoxic stress

1. Yanan Liu
2. Juanjuan Feng
3. Kun Yuan
4. Zhengzhen Wu
5. Longmiao Hu
6. Yue Lu
7. Kun Li
8. Jiawei Guo
9. Jing Chen
10. Chengbin Ma
11. Xiufeng Pang

• Curated by eLife

  Evaluation Summary:

  This research explored the role that BCL6 exerts on chemotherapy resistance in solid tumors other than previously reported hematological malignancies. The study also implicates the IFN-BCL6-PTEN axis as an antagonism target for overcoming resistance. This paper will be interesting to scientists who are specialists in cancer chemoresistance and oncological pharmacology.

  (This preprint has been reviewed by eLife. We include the public reviews from the reviewers here; the authors also receive private feedback with suggested changes to the manuscript. Reviewer #3 agreed to share their name with the authors.)

Reviewed by eLife

Comprehensive analysis of full-length transcripts reveals novel splicing abnormalities and oncogenic transcripts in liver cancer

1. Hiroki Kiyose
2. Hidewaki Nakagawa
3. Atsushi Ono
4. Hiroshi Aikata
5. Masaki Ueno
6. Shinya Hayami
7. Hiroki Yamaue
8. Kazuaki Chayama
9. Mihoko Shimada
10. Jing Hao Wong
11. Akihiro Fujimoto

Reviewed by Review Commons

Short senolytic or senostatic interventions rescue progression of radiation-induced frailty and premature ageing in mice

1. Edward Fielder
2. Tengfei Wan
3. Ghazaleh Alimohammadiha
4. Abbas Ishaq
5. Evon Low
6. B Melanie Weigand
7. George Kelly
8. Craig Parker
9. Brigid Griffin
10. Diana Jurk
11. Viktor I Korolchuk
12. Thomas von Zglinicki
13. Satomi Miwa

• Curated by eLife

  Evaluation Summary:

  This study evaluates the use of senolytics and senostatic agents on post-irradiation-induced frailty. The authors studied the effect of navitoclax, dasatinib/quercitin and metformin on several frailty measures, cognitive function, neuroinflammation, liver function to evaluate the therapeutic efficacy of these treatments. This manuscript has strong translational implications and will be of interest to those working in the aging and cancer therapy fields. This study provides potential new therapeutic options for those developing frailty after radiation treatment.

  (This preprint has been reviewed by eLife. We include the public reviews from the reviewers here; the authors also receive private feedback with suggested changes to the manuscript. The reviewers remained anonymous to the authors.)

Reviewed by eLife

Air pollution particles hijack peroxidasin to disrupt immunosurveillance and promote lung cancer

1. Zhenzhen Wang
2. Ziyu Zhai
3. Chunyu Chen
4. Xuejiao Tian
5. Zhen Xing
6. Panfei Xing
7. Yushun Yang
8. Junfeng Zhang
9. Chunming Wang
10. Lei Dong

• Curated by eLife

  Evaluation Summary:

  This is an interesting study that reveals a completely new mechanism by which inhaled fine particles may promote lung tumor development. The authors provide direct evidence that protein corona on those foreign objects can elicit such adverse effects. Their findings highlight the importance of the corona-endowed, 'new' bioactivity of nanomaterials in vivo - and even in a particular tissue-lungs.

  (This preprint has been reviewed by eLife. We include the public reviews from the reviewers here; the authors also receive private feedback with suggested changes to the manuscript. Reviewer #2 agreed to share their name with the authors.)

Reviewed by eLife