Cancer is an important public health problem worldwide. According to the latest global cancer burden update article using GLOBOCAN 2020, 19.3 million new cancer cases (18.1 million excluding nonmelanoma skin cancer) and nearly 10.0 million cancer deaths (9.9 million excluding nonmelanoma skin cancer) occurred worldwide in 2020 (1). On the other hand, since 1991, the cancer death rate has continuously decreased in some regions of the world, resulting in a 33% overall decrease and an estimated 3.8 million cancer deaths avoided in the United States of America (2). In particular, part of these improvements in survival is due to better knowledge of the molecular and cellular processes that drive cancer progression and metastasis, which has been fundamental in the development of targeted therapies for the treatment of cancer.
The current hallmarks of cancer encompass various characteristics such as evading growth suppressors; avoiding immune destruction; activating invasion and metastasis; senescent cells; genome instability and mutation; resisting cell death; and sustaining proliferative signaling (3). A better understanding of these cancer hallmarks and the molecular mechanisms that are responsible for these processes, will enable the development of effective and novel therapeutic modalities and improve the quality of life and survival of cancer patients. This Research Topic aimed to highlight recent advances in the field while emphasizing important directions and new possibilities for future inquiries.
In particular, Wang et al. reviewed the role of adipokines in pancreatic cancer. Adipokines are cytokines, such as leptin, adiponectin, and oncostatin-M, produced by adipose tissue that play functional roles in obesity, inflammation, the body’s energy/metabolic state, etc. (4). Leptin signaling increases MMP-13 synthesis, which promotes cell invasion and metastasis in human pancreatic cancer (5). Leptin also increases pancreatic tumor cell motility by activating the PI3K/AKT pathway (6). Likewise, adiponectin inhibits the growth of human pancreatic cancer by inhibiting the β-catenin signaling pathway (7), and oncostatin-M induces potent epithelial-mesenchymal transition and cancer stem cell phenotypes in pancreatic cancer (8).
In another article of this Research Topic, Zhou et al. reviewed patient-derived organoids (PDOs) in precision medicine. PDOs is a tool for individualized medical decisions that predicts patients’ reactions to therapy regimens and may enhance treatment results. Interestingly, Wnt-activated PDOs of Barrett’s esophagus exhibited histologic atypia, increased proliferative and replicative activity, decreased apoptosis, and longer cultivability (9).
In conclusion, molecular oncology represents a paradigm shift in cancer research, bringing together multidisciplinary efforts and cutting-edge technologies to tackle cancer at its core. This Research Topic provide a new update in this field that will direct further research to improve cancer prevention and treatment.
Statements
Author contributions
DB prepared the first version of the editorial. DB, JN and MC - discussed the editorial content and revised the final editorial text. All authors contributed to the article and approved the submitted version.
Funding
DB receives personal scholarship from Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq, Brazil).
Conflict of interest
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Publisher’s note
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
References
1
SungHFerlayJSiegelRLLaversanneMSoerjomataramIJemalAet al. Global cancer statistics 2020: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin (2021) 71(3):209–49. doi: 10.3322/caac.21660
2
SiegelRLMillerKDWagleNSJemalA. Cancer statistics, 2023. CA Cancer J Clin (2023) 73(1):17–48. doi: 10.3322/caac.21763
3
HanahanD. Hallmarks of cancer: new dimensions. Cancer Discovery (2022) 12(1):31–46. doi: 10.1158/2159-8290.CD-21-1059
4
OuchiNParkerJLLugusJJWalshK. Adipokines in inflammation and metabolic disease. Nat Rev Immunol (2011) 11(2):85–97. doi: 10.1038/nri2921
5
FanYGanYShenYCaiXSongYZhaoFet al. Leptin signaling enhances cell invasion and promotes the metastasis of human pancreatic cancer via increasing MMP-13 production. Oncotarget (2015) 6(18):16120–34. doi: 10.18632/oncotarget.3878
6
MendonsaAMChalfantMCGordenLDVanSaunMN. Modulation of the leptin receptor mediates tumor growth and migration of pancreatic cancer cells. PloS One (2015) 10(4):e0126686. doi: 10.1371/journal.pone.0126686
7
JiangJFanYZhangWShenYLiuTYaoMet al. Adiponectin suppresses human pancreatic cancer growth through attenuating the β-catenin signaling pathway. Int J Biol Sci (2019) 15(2):253–64. doi: 10.7150/ijbs.27420
8
SmigielJMParameswaranNJacksonMW. Potent EMT and CSC phenotypes are induced by oncostatin-m in pancreatic cancer. Mol Cancer Res (2017) 15(4):478–88. doi: 10.1158/1541-7786.MCR-16-0337
9
LiuXChengYAbrahamJMWangZWangZKeXet al. Modeling wnt signaling by CRISPR-Cas9 genome editing recapitulates neoplasia in human Barrett epithelial organoids. Cancer Lett (2018) 436:109–18. doi: 10.1016/j.canlet.2018.08.017
Summary
Keywords
cellular oncology, hallmarks of cancer, reviews - articles, targeted therapy, molecular oncology studies
Citation
Bezerra DP, Ni J and Chen M (2023) Editorial: Reviews in molecular and cellular oncology. Front. Oncol. 13:1224902. doi: 10.3389/fonc.2023.1224902
Received
18 May 2023
Accepted
01 June 2023
Published
08 June 2023
Volume
13 - 2023
Edited and reviewed by
Luisa Lanfrancone, European Institute of Oncology (IEO), Italy
Updates
Copyright
© 2023 Bezerra, Ni and Chen.
This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Daniel P. Bezerra, daniel.bezerra@fiocruz.br
Disclaimer
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.