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Biomedicines
Special Issues
Gastrointestinal Cancer Research: From Basic Science to the Clinic
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Gastrointestinal Cancer Research: From Basic Science to the Clinic

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (31 May 2021) | Viewed by 17316

Special Issue Editor

Dr. Yoku Hayakawa

E-Mail Website
Guest Editor
Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
Interests: gastrointestinal cancer; gastrointestinal stem cells; stem cell niche; metaplasia; signaling pathways; tumor microenvironment; mouse models
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue will focus on understanding the pathophysiology and molecular mechanisms that regulate gastrointestinal carcinogenesis as well as the tools that have been used in the past and are currently available for studying them both in vitro and in vivo. In particular, we will pay attention to the relevance and difference between mouse models and human pathogenesis in the gastrointestinal research field. This issue will include reviews, opinions, and short articles from experts in this research field, and cover broad topics such as important histopathological changes and/or key molecular pathways/factors during human and mouse gastric carcinogenesis, the role of gastrointestinal stem cells and their niche during cancer development, the cellular origin of gastrointestinal cancers, the tumor microenvironment in gastrointestinal cancers, advances in cell lines and primary organoids for GI research, epidemiological or endoscopic data analysis, and other related topics. We hope that the works in this issue will be helpful for solving unanswered questions in the clinic and advancing future basic and clinical studies.

Dr. Yoku Hayakawa
Guest Editor

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. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

  • gastric cancer
  • colon cancer
  • esophageal cancer
  • gastric stem cells
  • intestinal stem cells
  • metaplasia
  • tumor microenvironment
  • mouse model
  • organoid
  • signaling pathways
  • Helicobacter and other pathogens

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Related Special Issue

Published Papers (5 papers)

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Research

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14 pages, 8418 KiB  
Article
Regulation of Butyrate-Induced Resistance through AMPK Signaling Pathway in Human Colon Cancer Cells
by Hee Young Yoo, So Yeon Park, Sun-Young Chang and So Hee Kim
Biomedicines 2021, 9(11), 1604; https://doi.org/10.3390/biomedicines9111604 - 3 Nov 2021
Cited by 10 | Viewed by 2252
Abstract
Butyrates inhibit cell growth in colon cancer cells by inhibiting histone deacetylases. However, chronic exposure to butyrates induces butyrate resistance in colon cancer cells. The mechanism underlying the acquisition of resistance is not yet fully understood. Here, butyrate-resistant (BR) colon cancer cells were [...] Read more.
Butyrates inhibit cell growth in colon cancer cells by inhibiting histone deacetylases. However, chronic exposure to butyrates induces butyrate resistance in colon cancer cells. The mechanism underlying the acquisition of resistance is not yet fully understood. Here, butyrate-resistant (BR) colon cancer cells were developed in HCT116, HT29, and SW480 human colon cancer cells and were confirmed by the increase in the inhibitory concentrations of cell growth by 50% (IC50) compared to their respective parental (PT) cells. Chronic exposure to butyrate induced autophagy via higher expression of Beclin-1 and LC3B-II. The AMP-activated protein kinase (AMPK) was downregulated along with the activation of Akt and mammalian target of rapamycin (mTOR) and decrease in acetyl-CoA carboxylase (ACC) in BR colon cancer cells compared to those in their respective PT cells. Activation of AMPK by AICAR treatment in BR colon cancer cells suppressed cell proliferation by inhibiting Akt and mTOR and activating ACC. Taken together, chronic exposure to butyrate increased butyrate resistance in human colon cancer by inducing protective autophagy through the downregulation of AMPK/ACC and activation of Akt/mTOR signaling. Activation of AMPK restored sensitivity to butyrate by the inhibition of Akt/mTOR, suggesting that AMPK could be a therapeutic target for BR colon cancers. Full article
(This article belongs to the Special Issue Gastrointestinal Cancer Research: From Basic Science to the Clinic)
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18 pages, 3934 KiB  
Article
Combination of Mesenchymal Stem Cell-Delivered Oncolytic Virus with Prodrug Activation Increases Efficacy and Safety of Colorectal Cancer Therapy
by Chun-Te Ho, Mei-Hsuan Wu, Ming-Jen Chen, Shih-Pei Lin, Yu-Ting Yen and Shih-Chieh Hung
Biomedicines 2021, 9(5), 548; https://doi.org/10.3390/biomedicines9050548 - 13 May 2021
Cited by 15 | Viewed by 2915
Abstract
Although oncolytic viruses are currently being evaluated for cancer treatment in clinical trials, systemic administration is hindered by many factors that prevent them from reaching the tumor cells. When administered systemically, mesenchymal stem cells (MSCs) target tumors, and therefore constitute good cell carriers [...] Read more.
Although oncolytic viruses are currently being evaluated for cancer treatment in clinical trials, systemic administration is hindered by many factors that prevent them from reaching the tumor cells. When administered systemically, mesenchymal stem cells (MSCs) target tumors, and therefore constitute good cell carriers for oncolytic viruses. MSCs were primed with trichostatin A under hypoxia, which upregulated the expression of CXCR4, a chemokine receptor involved in tumor tropism, and coxsackievirus and adenovirus receptor that plays an important role in adenoviral infection. After priming, MSCs were loaded with conditionally replicative adenovirus that exhibits limited proliferation in cells with a functional p53 pathway and encodes Escherichia coli nitroreductase (NTR) enzymes (CRAdNTR) for targeting tumor cells. Primed MSCs increased tumor tropism and susceptibility to adenoviral infection, and successfully protected CRAdNTR from neutralization by anti-adenovirus antibodies both in vitro and in vivo, and specifically targeted p53-deficient colorectal tumors when infused intravenously. Analyses of deproteinized tissues by UPLC-MS/QTOF revealed that these MSCs converted the co-administered prodrug CB1954 into cytotoxic metabolites, such as 4-hydroxylamine and 2-amine, inducing oncolysis and tumor growth inhibition without being toxic for the host vital organs. This study shows that the combination of oncolytic viruses delivered by MSCs with the activation of prodrugs is a new cancer treatment strategy that provides a new approach for the development of oncolytic viral therapy for various cancers. Full article
(This article belongs to the Special Issue Gastrointestinal Cancer Research: From Basic Science to the Clinic)
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22 pages, 2892 KiB  
Article
Dietary Rice Bran-Modified Human Gut Microbial Consortia Confers Protection against Colon Carcinogenesis Following Fecal Transfaunation
by Kristopher D. Parker, Akhilendra K. Maurya, Hend Ibrahim, Sangeeta Rao, Petronella R. Hove, Dileep Kumar, Rama Kant, Bupinder Raina, Rajesh Agarwal, Kristine A. Kuhn, Komal Raina and Elizabeth P. Ryan
Biomedicines 2021, 9(2), 144; https://doi.org/10.3390/biomedicines9020144 - 3 Feb 2021
Cited by 22 | Viewed by 4114
Abstract
Rice bran, removed from whole grain rice for white rice milling, has demonstrated efficacy for the control and suppression of colitis and colon cancer in multiple animal models. Dietary rice bran intake was shown to modify human stool metabolites as a result of [...] Read more.
Rice bran, removed from whole grain rice for white rice milling, has demonstrated efficacy for the control and suppression of colitis and colon cancer in multiple animal models. Dietary rice bran intake was shown to modify human stool metabolites as a result of modifications to metabolism by gut microbiota. In this study, human stool microbiota from colorectal cancer (CRC) survivors that consumed rice bran daily was examined by fecal microbiota transplantation (FMT) for protection from azoxymethane and dextran sodium sulfate (AOM/DSS) induced colon carcinogenesis in germ-free mice. Mice transfaunated with rice bran-modified microbiota communities (RMC) harbored fewer neoplastic lesions in the colon and displayed distinct enrichment of Flavonifractor and Oscillibacter associated with colon health, and the depletion of Parabacteroides distasonis correlated with increased tumor burden. Two anti-cancer metabolites, myristoylcarnitine and palmitoylcarnitine were increased in the colon of RMC transplanted mice. Trimethylamine-N-oxide (TMAO) and tartarate that are implicated in CRC development were reduced in murine colon tissue after FMT with rice bran-modified human microbiota. Findings from this study show that rice bran modified gut microbiota from humans confers protection from colon carcinogenesis in mice and suggests integrated dietary-FMT intervention strategies should be tested for colorectal cancer control, treatment, and prevention. Full article
(This article belongs to the Special Issue Gastrointestinal Cancer Research: From Basic Science to the Clinic)
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11 pages, 1887 KiB  
Article
Distinct Features of Autoimmune Gastritis in Patients with Open-Type Chronic Gastritis in Japan
by Mayo Tsuboi, Ryota Niikura, Yoku Hayakawa, Yoshihiro Hirata, Tetsuo Ushiku and Kazuhiko Koike
Biomedicines 2020, 8(10), 419; https://doi.org/10.3390/biomedicines8100419 - 14 Oct 2020
Cited by 12 | Viewed by 3436
Abstract
In Asia, the incidences of Helicobacter pylori infection and gastric cancer are high, but their association with autoimmune gastritis (AIG) is unclear. This was a retrospective cohort study of patients endoscopically diagnosed with chronic gastritis between 2005 and 2017. AIG was diagnosed according [...] Read more.
In Asia, the incidences of Helicobacter pylori infection and gastric cancer are high, but their association with autoimmune gastritis (AIG) is unclear. This was a retrospective cohort study of patients endoscopically diagnosed with chronic gastritis between 2005 and 2017. AIG was diagnosed according to anti-parietal cell antibody positivity. Laboratory, histological findings, and gastric cancer incidence were compared between AIG and non-AIG patients. The AIG group had more females and a higher rate of thyroid disease. Serum levels of gastrin were significantly higher in AIG patients (mean 1412 and 353 pg/mL, p < 0.001). The endoscopic findings included a significantly higher percentage of corpus-dominant atrophy in AIG (31.67%) than in non-AIG (7.04%) patients (p < 0.001). Clusters of ECL cells were observed in 28% of AIG patients and 7% of non-AIG patients (p = 0.032). The cumulative incidence of gastric cancer at 5 and 10 years was 0% and 0.03% in the AIG group and 0.03% and 0.05% in the non-AIG group, and no significant difference in gastric cancer incidence was observed. Despite significant differences in gastrin levels between AIG and non-AIG patients, there was no evidence of an impact of AIG on the incidence of gastric cancer. Full article
(This article belongs to the Special Issue Gastrointestinal Cancer Research: From Basic Science to the Clinic)
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Review

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22 pages, 1953 KiB  
Review
Insights into Growth Factors in Liver Carcinogenesis and Regeneration: An Ongoing Debate on Minimizing Cancer Recurrence after Liver Resection
by Ana I. Álvarez-Mercado, Albert Caballeria-Casals, Carlos Rojano-Alfonso, Jesús Chávez-Reyes, Marc Micó-Carnero, Alfredo Sanchez-Gonzalez, Araní Casillas-Ramírez, Jordi Gracia-Sancho and Carmen Peralta
Biomedicines 2021, 9(9), 1158; https://doi.org/10.3390/biomedicines9091158 - 4 Sep 2021
Cited by 6 | Viewed by 3867
Abstract
Hepatocellular carcinoma has become a leading cause of cancer-associated mortality throughout the world, and is of great concern. Currently used chemotherapeutic drugs in the treatment of hepatocellular carcinoma lead to severe side effects, thus underscoring the need for further research to develop novel [...] Read more.
Hepatocellular carcinoma has become a leading cause of cancer-associated mortality throughout the world, and is of great concern. Currently used chemotherapeutic drugs in the treatment of hepatocellular carcinoma lead to severe side effects, thus underscoring the need for further research to develop novel and safer therapies. Liver resection in cancer patients is routinely performed. After partial resection, liver regeneration is a perfectly calibrated response apparently sensed by the body’s required liver function. This process hinges on the effect of several growth factors, among other molecules. However, dysregulation of growth factor signals also leads to growth signaling autonomy and tumor progression, so control of growth factor expression may prevent tumor progression. This review describes the role of some of the main growth factors whose dysregulation promotes liver tumor progression, and are also key in regenerating the remaining liver following resection. We herein summarize and discuss studies focused on partial hepatectomy and liver carcinogenesis, referring to hepatocyte growth factor, insulin-like growth factor, and epidermal growth factor, as well as their suitability as targets in the treatment of hepatocellular carcinoma. Finally, and given that drugs remain one of the mainstay treatment options in liver carcinogenesis, we have reviewed the current pharmacological approaches approved for clinical use or research targeting these factors. Full article
(This article belongs to the Special Issue Gastrointestinal Cancer Research: From Basic Science to the Clinic)
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