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Inflammation and Cancer 2023
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Inflammation and Cancer 2023

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (15 April 2024) | Viewed by 6219

Special Issue Editors

Prof. Dr. Takuji Tanaka

E-Mail Website
Guest Editor
Department of Diagnostic Pathology and Research Center of Diagnostic Pathology, Gifu Municipal Hospital, 7-1 Kashima-cho, Gifu 500-8513, Japan
Interests: colorectal carcinogenesis; cancer chemiprevention; inflammatory bowel disease; ulcerative colitis; Crohn’s disease; animal model
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Masahito Shimizu

E-Mail Website
Guest Editor
First Department of Internal Medicine, Gifu University Hospital, Gifu 501-1194, Japan
Interests: liver carcinogenesis; cancer chemoprevention; chronic hepatitis; metabolic syndrome; retinoid; phytochemicals; clinical trial
Special Issues, Collections and Topics in MDPI journals
Dr. Michihiro Mutoh

E-Mail Website
Guest Editor
1. Department of Molecular-Targeting Prevention, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan
2. Epidemiology and Prevention Division, Center for Public Health Sciences, National Cancer Center, Tokyo 104-0045, Japan
Interests: cancer prevention; animal models; translational research
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Based on the data that are now available in the GLOBOCAN series of the IARC, there were 14.1 million new cases of cancer and 8.2 million cancer deaths in 2012. Among epithelial malignancies, some cancers have strong links to chronic inflammation and develop in the background of uncontrolled chronic inflammation.

Recent scientific advances have greatly contributed to the dissection of the complex molecular and cellular pathways involved in the connection between cancer and inflammation. The decreased incidence of tumors in individuals who have used non-steroidal anti-inflammatory drugs is supportive of certain role for inflammation in cancer susceptibility. Inflammatory cells and mediators are essential components in the tumor microenvironment and play decisive roles in the initiation, promotion and progression of cancer, including epithelial-to-mesenchymal transition (EMT) and metastasis.

Activation of inflammasomes, which are large protein complexes, plays a critical role during inflammation by producing cytokines. The activation of inflammasomes plays diverse and sometimes contrasting roles in cancer promotion and therapy, depending on the specific context. Recent studies have shown that autophagy, an intracellular degradation system associated with maintenance of cellular homeostasis, plays a key role in inflammasome inactivation. Meanwhile, autophagy is induced upon progression of various human cancers to metastasis. Thus, major players in inflammation may be a double-edged sword for carcinogenesis. In this context, appropriate strategies will be required to prevent cancer.

In light of this, this Special Issue, entitled “Inflammation and Cancer 2023”, is well-timed to say the least, and provides a practical appreciation for the many biochemical, molecular, immunological, and cellular mechanisms shared by cancer and inflammatory processes.

Prof. Dr. Takuji Tanaka
Prof. Dr. Masahito Shimizu
Dr. Michihiro Mutoh
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

 

Keywords

  • inflammation
  • cytokines
  • gut microbiota
  • insulin resistance
  • molecular biology
  • autophagy
  • epithelial-to-mesenchymal transition (EMT)
  • tumor microenvironment
 

Related Special Issues

Published Papers (5 papers)

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Research

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20 pages, 4642 KiB  
Article
Prostaglandin E2 Exposure Disrupts E-Cadherin/Caveolin-1-Mediated Tumor Suppression to Favor Caveolin-1-Enhanced Migration, Invasion, and Metastasis in Melanoma Models
by Lorena Lobos-González, Lorena Oróstica, Natalia Díaz-Valdivia, Victoria Rojas-Celis, America Campos, Eduardo Duran-Jara, Nicole Farfán, Lisette Leyton and Andrew F. G. Quest
Int. J. Mol. Sci. 2023, 24(23), 16947; https://doi.org/10.3390/ijms242316947 - 29 Nov 2023
Viewed by 857
Abstract
Caveolin-1 (CAV1) is a membrane-bound protein that suppresses tumor development yet also promotes metastasis. E-cadherin is important in CAV1-dependent tumor suppression and prevents CAV1-enhanced lung metastasis. Here, we used murine B16F10 and human A375 melanoma cells with low levels of endogenous CAV1 and [...] Read more.
Caveolin-1 (CAV1) is a membrane-bound protein that suppresses tumor development yet also promotes metastasis. E-cadherin is important in CAV1-dependent tumor suppression and prevents CAV1-enhanced lung metastasis. Here, we used murine B16F10 and human A375 melanoma cells with low levels of endogenous CAV1 and E-cadherin to unravel how co-expression of E-cadherin modulates CAV1 function in vitro and in vivo in WT C57BL/6 or Rag−/− immunodeficient mice and how a pro-inflammatory environment generated by treating cells with prostaglandin E2 (PGE2) alters CAV1 function in the presence of E-cadherin. CAV1 expression augmented migration, invasion, and metastasis of melanoma cells, and these effects were abolished via transient co-expression of E-cadherin. Importantly, exposure of cells to PGE2 reverted the effects of E-cadherin expression and increased CAV1 phosphorylation on tyrosine-14 and metastasis. Moreover, PGE2 administration blocked the ability of the CAV1/E-cadherin complex to prevent tumor formation. Therefore, our results support the notion that PGE2 can override the tumor suppressor potential of the E-cadherin/CAV1 complex and that CAV1 released from the complex is phosphorylated on tyrosine-14 and promotes migration/invasion/metastasis. These observations provide direct evidence showing how a pro-inflammatory environment caused here via PGE2 administration can convert a potent tumor suppressor complex into a promoter of malignant cell behavior. Full article
(This article belongs to the Special Issue Inflammation and Cancer 2023)
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11 pages, 1554 KiB  
Article
A Novel Mouse Model of Intrahepatic Cholangiocarcinoma Induced by Azoxymethane
by Yohei Shirakami, Junichi Kato, Masaya Ohnishi, Daisuke Taguchi, Toshihide Maeda, Takayasu Ideta, Masaya Kubota, Hiroyasu Sakai, Hiroyuki Tomita, Takuji Tanaka and Masahito Shimizu
Int. J. Mol. Sci. 2023, 24(19), 14581; https://doi.org/10.3390/ijms241914581 - 26 Sep 2023
Viewed by 911
Abstract
Cholangiocarcinoma is the second most common primary cancer of the liver and has a poor prognosis. Various animal models, including carcinogen-induced and genetically engineered rodent models, have been established to clarify the mechanisms underlying cholangiocarcinoma development. In the present study, we developed a [...] Read more.
Cholangiocarcinoma is the second most common primary cancer of the liver and has a poor prognosis. Various animal models, including carcinogen-induced and genetically engineered rodent models, have been established to clarify the mechanisms underlying cholangiocarcinoma development. In the present study, we developed a novel mouse model of malignant lesions in the biliary ducts induced by the administration of the carcinogen azoxymethane to obese C57BLKS/J-db/db mice. A histopathological analysis revealed that the biliary tract lesions in the liver appeared to be an intrahepatic cholangiocarcinoma with higher tumor incidence, shorter experimental duration, and a markedly increased incidence in obese mice. Molecular markers analyzed using a microarray and a qPCR indicated that the cancerous lesions originated from the cholangiocytes and developed in the inflamed livers. These findings indicated that this is a novel mouse model of intrahepatic cholangiocarcinoma in the context of steatohepatitis. This model can be used to provide a better understanding of the pathogenic mechanisms of cholangiocarcinoma and to develop novel therapeutic strategies for this malignancy. Full article
(This article belongs to the Special Issue Inflammation and Cancer 2023)
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15 pages, 11315 KiB  
Article
A Short-Term Model of Colitis-Associated Colorectal Cancer That Suggests Initial Tumor Development and the Characteristics of Cancer Stem Cells
by Yasushi Matsumoto, Toshiro Fukui, Shunsuke Horitani, Yuji Tanimura, Ryo Suzuki, Takashi Tomiyama, Yusuke Honzawa, Tomomitsu Tahara, Kazuichi Okazaki and Makoto Naganuma
Int. J. Mol. Sci. 2023, 24(14), 11697; https://doi.org/10.3390/ijms241411697 - 20 Jul 2023
Cited by 1 | Viewed by 1157
Abstract
The mechanisms underlying the transition from colitis-associated inflammation to carcinogenesis and the cell origin of cancer formation are still unclear. The azoxymethane (AOM)/dextran sodium sulfate (DSS) mouse model reproduces human colitis-associated colorectal cancer. To elucidate the mechanisms of cancer development and dynamics of [...] Read more.
The mechanisms underlying the transition from colitis-associated inflammation to carcinogenesis and the cell origin of cancer formation are still unclear. The azoxymethane (AOM)/dextran sodium sulfate (DSS) mouse model reproduces human colitis-associated colorectal cancer. To elucidate the mechanisms of cancer development and dynamics of the linker threonine-phosphorylated Smad2/3 (pSmad2/3L-Thr)-positive cells, we explored the early stages of colitis-associated colorectal cancer in AOM/DSS mice. The AOM/DSS mice were sacrificed at 4 to 6 weeks following AOM administration. To analyze the initial lesions, immunofluorescence staining for the following markers was performed: β-catenin, Ki67, CDK4, Sox9, Bmi1, cyclin D1, and pSmad2/3L-Thr. Micro-neoplastic lesions were flat and unrecognizable, and the uni-cryptal ones were either open to the surfaces or hidden within the mucosae. These neoplastic cells overexpressed β-catenin, Sox9, Ki67, and Cyclin D1 and had large basophilic nuclei in the immature atypical cells. In both the lesions, pSmad2/3L-Thr-positive cells were scattered and showed immunohistochemical co-localization with β-catenin, CDK4, and Bmi1 but never with Ki67. More β-catenin-positive neoplastic cells of both lesions were detected at the top compared to the base or center of the mucosae. We confirmed initial lesions in the colitis-associated colorectal cancer model mice and observed results that suggest that pSmad2/3L-Thr is a biomarker for tissue stem cells and cancer stem cells. Full article
(This article belongs to the Special Issue Inflammation and Cancer 2023)
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Review

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32 pages, 2212 KiB  
Review
Diagnostic Challenges during Inflammation and Cancer: Current Biomarkers and Future Perspectives in Navigating through the Minefield of Reactive versus Dysplastic and Cancerous Lesions in the Digestive System
by Ioannis S. Pateras, Ana Igea, Ilias P. Nikas, Danai Leventakou, Nektarios I. Koufopoulos, Argyro Ioanna Ieronimaki, Anna Bergonzini, Han Suk Ryu, Antonios Chatzigeorgiou, Teresa Frisan, Christos Kittas and Ioannis G. Panayiotides
Int. J. Mol. Sci. 2024, 25(2), 1251; https://doi.org/10.3390/ijms25021251 - 19 Jan 2024
Cited by 1 | Viewed by 1037
Abstract
In the setting of pronounced inflammation, changes in the epithelium may overlap with neoplasia, often rendering it impossible to establish a diagnosis with certainty in daily clinical practice. Here, we discuss the underlying molecular mechanisms driving tissue response during persistent inflammatory signaling along [...] Read more.
In the setting of pronounced inflammation, changes in the epithelium may overlap with neoplasia, often rendering it impossible to establish a diagnosis with certainty in daily clinical practice. Here, we discuss the underlying molecular mechanisms driving tissue response during persistent inflammatory signaling along with the potential association with cancer in the gastrointestinal tract, pancreas, extrahepatic bile ducts, and liver. We highlight the histopathological challenges encountered in the diagnosis of chronic inflammation in routine practice and pinpoint tissue-based biomarkers that could complement morphology to differentiate reactive from dysplastic or cancerous lesions. We refer to the advantages and limitations of existing biomarkers employing immunohistochemistry and point to promising new markers, including the generation of novel antibodies targeting mutant proteins, miRNAs, and array assays. Advancements in experimental models, including mouse and 3D models, have improved our understanding of tissue response. The integration of digital pathology along with artificial intelligence may also complement routine visual inspections. Navigating through tissue responses in various chronic inflammatory contexts will help us develop novel and reliable biomarkers that will improve diagnostic decisions and ultimately patient treatment. Full article
(This article belongs to the Special Issue Inflammation and Cancer 2023)
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20 pages, 2225 KiB  
Review
The Therapeutic Potential of CDK4/6 Inhibitors, Novel Cancer Drugs, in Kidney Diseases
by Xuan-Bing Liang, Zhi-Cheng Dai, Rong Zou, Ji-Xin Tang and Cui-Wei Yao
Int. J. Mol. Sci. 2023, 24(17), 13558; https://doi.org/10.3390/ijms241713558 - 31 Aug 2023
Viewed by 1383
Abstract
Inflammation is a crucial pathological feature in cancers and kidney diseases, playing a significant role in disease progression. Cyclin-dependent kinases CDK4 and CDK6 not only contribute to cell cycle progression but also participate in cell metabolism, immunogenicity and anti-tumor immune responses. Recently, CDK4/6 [...] Read more.
Inflammation is a crucial pathological feature in cancers and kidney diseases, playing a significant role in disease progression. Cyclin-dependent kinases CDK4 and CDK6 not only contribute to cell cycle progression but also participate in cell metabolism, immunogenicity and anti-tumor immune responses. Recently, CDK4/6 inhibitors have gained approval for investigational treatment of breast cancer and various other tumors. Kidney diseases and cancers commonly exhibit characteristic pathological features, such as the involvement of inflammatory cells and persistent chronic inflammation. Remarkably, CDK4/6 inhibitors have demonstrated impressive efficacy in treating non-cancerous conditions, including certain kidney diseases. Current studies have identified the renoprotective effect of CDK4/6 inhibitors, presenting a novel idea and potential direction for treating kidney diseases in the future. In this review, we briefly reviewed the cell cycle in mammals and the role of CDK4/6 in regulating it. We then provided an introduction to CDK4/6 inhibitors and their use in cancer treatment. Additionally, we emphasized the importance of these inhibitors in the treatment of kidney diseases. Collectively, growing evidence demonstrates that targeting CDK4 and CDK6 through CDK4/6 inhibitors might have therapeutic benefits in various cancers and kidney diseases and should be further explored in the future. Full article
(This article belongs to the Special Issue Inflammation and Cancer 2023)
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