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Molecular Mechanisms, Diagnosis and Treatments in Digestive Malignancy

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (1 June 2020) | Viewed by 39526

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Dr. Tatsuo Kanda

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Division of Gastroenterology and Hepatology, Department of Internal Medicine, Nihon University School of Medicine, 30-1 Oyaguchi-Kamicho, Itabashi-ku, Tokyo 173-8610, Japan
Interests: viral hepatitis; hepatocellular carcinoma; innate immunity; unfolded protein response
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Assist. Prof. Ryota Masuzaki, M.D.

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Division of Liver Transplantation, Department of Surgery Vanderbilt University Medical Center, 2213 Garland Ave. MRB4, Rm10425, Nashville, TN 37232, USA
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Dr. Reina Sasaki, M.D.

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Department of Pathology, Saint Louis University, St. Louis, MO 63104, USA

Prof. Dr. Mitsuhiko Moriyama

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Division of Gastroenterology and Hepatology, Department of Internal Medicine, Nihon University School of Medicine, 30-1 Oyaguchi-Kamicho, Itabashi-ku, Tokyo 173-8610, Japan
Interests: hepatitis; trace element; cancer
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Prof. Dr. Ratna B. Ray, Ph.D.

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Department of Pathology, Saint Louis University, St. Louis, MO 63104, USA

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Dear Colleagues,

Cancer is a leading cause of death in the world. In 2018, the World Health Organization reported that colorectal and stomach cancers are ones of common cancers, with an estimated 1.8 million cases and 1.03 million cases annually, respectively. Common causes of cancer death are colorectal (862,000 deaths), stomach (783,000 deaths) and liver (782,000 deaths) cancers. Recently, nucleos(t)ide analogues and direct acting antiviral agents (DAAs) have been available for hepatitis B virus (HBV) and hepatitis C virus (HCV), respectively. These drugs are known to control the replication of hepatitis viruses. However, the mechanism of progression of liver fibrosis and occurrence and recurrence of hepatocellular carcinoma is still largely unknown. Treatments for other liver diseases, including alcoholic liver injury and non-alcoholic steatosis are also being developed.

The mechanisms of other digestive malignancies, including biliary tract cancer, pancreatic cancer and gastrointestinal tract cancer, should be further elucidated, leading to the development of new drugs for these diseases and improvements in patient prognosis and survival. Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies, with an overall median survival period of 4.6 months and an overall median 5-year survival rate of 3%. Many factors contribute to the development of PDAC, poor prognosis of PDAC and chemoresistance. The mechanisms of the progression of fibrosis and carcinogens are still largely unknown. The mechanisms of the pathogenesis of tumors in the gallbladder and those in the bile duct are also unknown.

Gastrointestinal tract cancer is very common and one of the major causes of mortality worldwide. Both genetic and environmental factors contribute to the onset of cancer. Several epidemiological studies suggest that diet may play an important role in the etiology of digestive tract cancer. Intestinal bacteria, which can influence the immune system and health conditions, are known to cause the development and progression of gastrointestinal tract neoplasms. Ulcerative colitis (UC) is also known to develop UC-associated colon cancers and colitic cancers through the inflammation–dysplasia sequence. Recent studies using genome-wide association studies (GWAS) have facilitated the identification of multiple replicable common genetic variations associated with cancers, including pancreatic cancers and colorectal cancer. It is hoped that these recent studies will contribute to the development of new treatments and improve of patient prognosis and survival.

In this Special Issue, we focus on recent basic and clinical cancer research into digestive malignancy.

Assoc. Prof. Tatsuo Kanda, M.D.

Assist. Prof. Ryota Masuzaki, M.D.
Dr. Reina Sasaki, M.D.
Prof. Dr. Mitsuhiko Moriyama, M.D.
Prof. Dr. Ratna B. Ray, Ph.D.
Guest Editors

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Keywords

liver
biliary tract
pancreas
stomach
fibrosis
malignancy

Published Papers (11 papers)

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Editorial

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4 pages, 192 KiB

Open AccessEditorial

Molecular Mechanisms, Diagnosis and Treatments in Digestive Malignancy

by Tatsuo Kanda, Ryota Masuzaki, Reina Sasaki-Tanaka, Hirofumi Kogure and Mitsuhiko Moriyama

Int. J. Mol. Sci. 2023, 24(7), 6471; https://doi.org/10.3390/ijms24076471 - 30 Mar 2023

Viewed by 933

Abstract

In this Special Issue, “Molecular Mechanisms, Diagnosis and Treatments in Digestive Malignancy”, of the International Journal of Molecular Sciences, a total of 10 impactful articles have been published [...] Full article

(This article belongs to the Special Issue Molecular Mechanisms, Diagnosis and Treatments in Digestive Malignancy)

Research

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28 pages, 1514 KiB

Open AccessArticle

MicroRNA Profiling in Oesophageal Adenocarcinoma Cell Lines and Patient Serum Samples Reveals a Role for miR-451a in Radiation Resistance

by Frederike Butz, Ann-Kathrin Eichelmann, George C. Mayne, Tingting Wang, Isabell Bastian, Karen Chiam, Shashikanth Marri, Pamela J. Sykes, Bas P. Wijnhoven, Eelke Toxopeus, Michael Z. Michael, Christos S. Karapetis, Richard Hummel, David I. Watson and Damian J. Hussey

Int. J. Mol. Sci. 2020, 21(23), 8898; https://doi.org/10.3390/ijms21238898 - 24 Nov 2020

Cited by 9 | Viewed by 2614

Abstract

Many patients with Oesophageal Adenocarcinoma (OAC) do not benefit from chemoradiotherapy treatment due to therapy resistance. To better understand the mechanisms involved in resistance and to find potential biomarkers, we investigated the association of microRNAs, which regulate gene expression, with the response to individual treatments, focusing on radiation. Intrinsic radiation resistance and chemotherapy drug resistance were assessed in eight OAC cell lines, and miRNA expression profiling was performed via TaqMan OpenArray qPCR. miRNAs discovered were either uniquely associated with resistance to radiation, cisplatin, or 5-FU, or were common to two or all three of the treatments. Target mRNA pathway analyses indicated several potential mechanisms of treatment resistance. miRNAs associated with the in vitro treatment responses were then investigated for association with pathologic response to neoadjuvant chemoradiotherapy (nCRT) in pre-treatment serums of patients with OAC. miR-451a was associated uniquely with resistance to radiation treatment in the cell lines, and with the response to nCRT in patient serums. Inhibition of miR-451a in the radiation resistant OAC cell line OE19 increased radiosensitivity (Survival Fraction 73% vs. 87%, p = 0.0003), and altered RNA expression. Pathway analysis of effected small non-coding RNAs and corresponding mRNA targets suggest potential mechanisms of radiation resistance in OAC. Full article

(This article belongs to the Special Issue Molecular Mechanisms, Diagnosis and Treatments in Digestive Malignancy)

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13 pages, 5242 KiB

Open AccessArticle

Glucagon-Like Peptide-1 Receptor Agonist Prevented the Progression of Hepatocellular Carcinoma in a Mouse Model of Nonalcoholic Steatohepatitis

by Motoyasu Kojima, Hirokazu Takahashi, Takuya Kuwashiro, Kenichi Tanaka, Hitoe Mori, Iwata Ozaki, Yoichiro Kitajima, Yayoi Matsuda, Kenji Ashida, Yuichiro Eguchi and Keizo Anzai

Int. J. Mol. Sci. 2020, 21(16), 5722; https://doi.org/10.3390/ijms21165722 - 10 Aug 2020

Cited by 29 | Viewed by 3526

Abstract

Glucagon-like peptide-1 (GLP-1) receptor agonists are used to treat diabetes, but their effects on nonalcoholic steatohepatitis (NASH) and the development of hepatocellular carcinoma (HCC) remain unclear. In this study, mice with streptozotocin- and high-fat diet-induced diabetes and NASH were subcutaneously treated with liraglutide or saline (control) for 14 weeks. Glycemic control, hepatocarcinogenesis, and liver histology were compared between the groups. Fasting blood glucose levels were significantly lower in the liraglutide group than in the control group (210.0 ± 17.3 mg/dL vs. 601.8 ± 123.6 mg/dL), and fasting insulin levels were significantly increased by liraglutide (0.18 ± 0.06 ng/mL vs. 0.09 ± 0.03 ng/mL). Liraglutide completely suppressed hepatocarcinogenesis, whereas HCC was observed in all control mice (average tumor count, 5.5 ± 3.87; average tumor size, 8.1 ± 5.0 mm). Liraglutide significantly ameliorated steatosis, inflammation, and hepatocyte ballooning of non-tumorous lesions in the liver compared with the control findings, and insulin-positive β-cells were observed in the pancreas in liraglutide-treated mice but not in control mice. In conclusion, liraglutide ameliorated NASH and suppressed hepatocarcinogenesis in diabetic mice. GLP-1 receptor agonists can be used to improve the hepatic outcome of diabetes. Full article

(This article belongs to the Special Issue Molecular Mechanisms, Diagnosis and Treatments in Digestive Malignancy)

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10 pages, 2838 KiB

Open AccessArticle

NRF2 Knockdown Resensitizes 5-Fluorouracil-Resistant Pancreatic Cancer Cells by Suppressing HO-1 and ABCG2 Expression

by Eui Joo Kim, Yoon Jae Kim, Hye In Lee, Seok-Hoo Jeong, Hyo Jung Nam and Jae Hee Cho

Int. J. Mol. Sci. 2020, 21(13), 4646; https://doi.org/10.3390/ijms21134646 - 30 Jun 2020

Cited by 21 | Viewed by 3090

Abstract

Chemoresistance is a leading cause of morbidity and mortality in patients with pancreatic cancer and remains an obstacle to successful treatment. The antioxidant transcription factor nuclear factor (erythroid-derived 2)-related factor 2 (NRF2), which plays important roles in tumor angiogenesis and invasiveness, is upregulated in pancreatic ductal adenocarcinoma (PDAC), where it correlates with poor survival. Here, we investigated the role of NRF2 in two 5-Fluourouracil-resistant (5-FUR) PDAC cell lines: BxPC-3 and CFPAC-1. Levels of NRF2 and antioxidants, such as heme oxygenase 1 (HO-1), NAD(P)H quinone dehydrogenase 1 (NQO1), and superoxide dismutase 2 (SOD2), were higher in the chemoresistant cells than in their chemosensitive counterparts. Expression of epithelial mesenchymal transition (EMT) markers, stemness markers, including Nanog, Oct4, and CD133, and that of the drug transporter ATP binding cassette, subfamily G, member A2 (ABCG2) was also upregulated in 5-FUR PDAC cells. NRF2 knockdown reversed 5-FU resistance of PDAC cells via suppression of ABCG2 and HO-1. In summary, these data indicate that NRF2 is a potential target for resensitizing 5-FUR PDAC cells to 5-FU to improve treatment outcomes in patients with pancreatic cancer. Full article

(This article belongs to the Special Issue Molecular Mechanisms, Diagnosis and Treatments in Digestive Malignancy)

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12 pages, 4492 KiB

Open AccessArticle

Different Mechanisms of Action of Regorafenib and Lenvatinib on Toll-Like Receptor-Signaling Pathways in Human Hepatoma Cell Lines

by Reina Sasaki, Tatsuo Kanda, Mariko Fujisawa, Naoki Matsumoto, Ryota Masuzaki, Masahiro Ogawa, Shunichi Matsuoka, Kazumichi Kuroda and Mitsuhiko Moriyama

Int. J. Mol. Sci. 2020, 21(9), 3349; https://doi.org/10.3390/ijms21093349 - 09 May 2020

Cited by 22 | Viewed by 3239

Abstract

Multiple kinase inhibitors are available for patients with advanced hepatocellular carcinoma (HCC). It is largely unknown whether regorafenib or lenvatinib modulates innate immunity including Toll-like receptor (TLR)-signaling pathways in HCC. We performed real-time RT-PCR to investigate 84 TLR-associated gene expression levels and compared these gene expression levels in each hepatoma cells treated with or without regorafenib or lenvatinib. In response to regorafenib, nine and 10 genes were upregulated in Huh7 and HepG2 cells, respectively, and only C-X-C motif chemokine ligand 10 was upregulated in both cell lines. A total of 14 and 12 genes were downregulated in Huh7 and HepG2 cells, respectively, and two genes (Fos proto-oncogene, AP-1 transcription factor subunit, and ubiquitin conjugating enzyme E2 N) were downregulated in both cell lines. In response to lenvatinib, four and 16 genes were upregulated in Huh7 and HepG2 cells, respectively, and two genes (interleukin 1 alpha and TLR4) were upregulated in both cells. Six and one genes were downregulated in Huh7 and HepG2, respectively, and no genes were downregulated in both cell lines. In summary, regorafenib and lenvatinib affect TLR signaling pathways in human hepatoma cell lines. Modulation of TLR signaling pathway may improve the treatment of HCC patients with refractory disease. Full article

(This article belongs to the Special Issue Molecular Mechanisms, Diagnosis and Treatments in Digestive Malignancy)

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10 pages, 1087 KiB

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On-treatment Serum Mac-2 Binding Protein Glycosylation Isomer (M2BPGi) Level and Risk of Hepatocellular Carcinoma Development in Patients with Chronic Hepatitis B during Nucleot(s)ide Analogue Therapy

by Ayato Murata, Nozomi Amano, Sho Sato, Hironori Tsuzura, Ko Tomishima, Shunsuke Sato, Kohei Matsumoto, Yuji Shimada, Katsuyori Iijima and Takuya Genda

Int. J. Mol. Sci. 2020, 21(6), 2051; https://doi.org/10.3390/ijms21062051 - 17 Mar 2020

Cited by 7 | Viewed by 2558

Abstract

We aimed to analyze the serum level of a novel fibrosis marker, Mac-2-binding protein glycosylation isomer (M2BPGi), and its predictive value for hepatocellular carcinoma (HCC) development in chronic hepatitis B (CHB) under nucleot(s)ide analogue (NA) therapy. Serum M2BPGi levels were quantified in 147 CHB patients at baseline, 48 weeks after starting NA therapy, and at the patients’ last visit. The serum M2BPGi level serially decreased at each time point. During the median follow-up time of 6.6 years, 14 of 147 patients developed HCC. Multivariate Cox proportional hazard analysis demonstrated that high serum M2BPGi at 48 weeks was an independent risk factor for HCC development. A cutoff value of M2BPGi at 48 weeks > 1.5 showed an adjusted hazard ratio = 34.9 (95% confidence interval, 4.3–284.9). The 3- and 5-year cumulative incidence of HCC in patients with low M2BPGi were 0.9% and 4.2%, respectively, whereas those in patients with high M2BPGi were 10.1% and 25.6%, respectively (p < 0.001). In conclusion, Serum M2BPGi level at 48 weeks is a useful predictor for HCC development in patients with CHB who receive NA therapy. Full article

(This article belongs to the Special Issue Molecular Mechanisms, Diagnosis and Treatments in Digestive Malignancy)

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14 pages, 2071 KiB

Open AccessArticle

Telmisartan Inhibits Cell Proliferation and Tumor Growth of Esophageal Squamous Cell Carcinoma by Inducing S-Phase Arrest In Vitro and In Vivo

by Takanori Matsui, Taiga Chiyo, Hideki Kobara, Shintaro Fujihara, Koji Fujita, Daisuke Namima, Mai Nakahara, Nobuya Kobayashi, Noriko Nishiyama, Tatsuo Yachida, Asahiro Morishita, Hisakazu Iwama and Tsutomu Masaki

Int. J. Mol. Sci. 2019, 20(13), 3197; https://doi.org/10.3390/ijms20133197 - 29 Jun 2019

Cited by 31 | Viewed by 3924

Abstract

Esophageal squamous cell carcinoma (ESCC) is the most common primary esophageal malignancy. Telmisartan, an angiotensin II type 1 (AT1) receptor blocker (ARB) and a widely used antihypertensive, has been shown to inhibit proliferation of various cancer types. This study evaluated the effects of telmisartan on human ESCC cell proliferation in vitro and in vivo and sought to identify the microRNAs (miRNAs) involved in these antitumor effects. We examined the effects of telmisartan on three human ESCC cell lines (KYSE150, KYSE180, and KYSE850). Telmisartan inhibited proliferation of these three cell lines by inducing S-phase arrest, which was accompanied by decreased expression of cyclin A2, cyclin-dependent kinase 2, and other cell cycle-related proteins. Additionally, telmisartan reduced levels of phosphorylated ErbB3 and thrombospondin-1 in KYSE180 cells. Furthermore, expression of miRNAs was remarkably altered by telmisartan in vitro. Telmisartan also inhibited tumor growth in vivo in a xenograft mouse model. In conclusion, telmisartan inhibited cell proliferation and tumor growth in ESCC cells by inducing cell-cycle arrest. Full article

(This article belongs to the Special Issue Molecular Mechanisms, Diagnosis and Treatments in Digestive Malignancy)

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Review

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16 pages, 1844 KiB

Open AccessReview

Molecular Mechanisms and Treatment of Sarcopenia in Liver Disease: A Review of Current Knowledge

by Hiroteru Kamimura, Takeki Sato, Kazuki Natsui, Takamasa Kobayashi, Tomoaki Yoshida, Kenya Kamimura, Atsunori Tsuchiya, Toshiko Murayama, Junji Yokoyama, Hirokazu Kawai, Masaaki Takamura and Shuji Terai

Int. J. Mol. Sci. 2021, 22(3), 1425; https://doi.org/10.3390/ijms22031425 - 31 Jan 2021

Cited by 10 | Viewed by 5192

Abstract

Sarcopenia is characterized by progressive and generalized loss of skeletal muscle mass and strength that occurs with aging or in association with various diseases. The condition is prevalent worldwide and occurs more frequently in patients with chronic diseases owing to the intrinsic relationship of muscles with glucose, lipid, and protein metabolism. Liver cirrhosis is characterized by the progression of necro-inflammatory liver diseases, which leads to fibrosis, portal hypertension, and a catabolic state, which causes loss of muscle tissue. Sarcopenia is of significant concern in the state of liver cirrhosis because sarcopenia has been associated with higher mortality, increased hospital admissions, worse post-liver transplant outcomes, decreased quality of life, and increased risk for other complications associated with cirrhosis. Therefore, sarcopenia is also an important feature of liver cirrhosis, representing a negative prognostic factor and influencing mortality. An increased understanding of sarcopenia could lead to the development of novel therapeutic approaches that could help improve the cognitive impairment of cirrhotic patients; therefore, we present a review of the mechanisms and diagnosis of sarcopenia in liver disease and existing therapeutic approaches. Full article

(This article belongs to the Special Issue Molecular Mechanisms, Diagnosis and Treatments in Digestive Malignancy)

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18 pages, 637 KiB

Open AccessReview

Noninvasive Assessment of Liver Fibrosis: Current and Future Clinical and Molecular Perspectives

by Ryota Masuzaki, Tatsuo Kanda, Reina Sasaki, Naoki Matsumoto, Masahiro Ogawa, Shunichi Matsuoka, Seth J. Karp and Mitsuhiko Moriyama

Int. J. Mol. Sci. 2020, 21(14), 4906; https://doi.org/10.3390/ijms21144906 - 11 Jul 2020

Cited by 21 | Viewed by 4651

Abstract

Liver fibrosis is one of the risk factors for hepatocellular carcinoma (HCC) development. The staging of liver fibrosis can be evaluated only via a liver biopsy, which is an invasive procedure. Noninvasive methods for the diagnosis of liver fibrosis can be divided into morphological tests such as elastography and serum biochemical tests. Transient elastography is reported to have excellent performance in the diagnosis of liver fibrosis and has been accepted as a useful tool for the prediction of HCC development and other clinical outcomes. Two-dimensional shear wave elastography is a new technique and provides a real-time stiffness image. Serum fibrosis markers have been studied based on the mechanism of fibrogenesis and fibrolysis. In the healthy liver, homeostasis of the extracellular matrix is maintained directly by enzymes called matrix metalloproteinases (MMPs) and their specific inhibitors, tissue inhibitors of metalloproteinases (TIMPs). MMPs and TIMPs could be useful serum biomarkers for liver fibrosis and promising candidates for the treatment of liver fibrosis. Further studies are required to establish liver fibrosis-specific markers based on further clinical and molecular research. In this review, we summarize noninvasive fibrosis tests and molecular mechanism of liver fibrosis in current daily clinical practice. Full article

(This article belongs to the Special Issue Molecular Mechanisms, Diagnosis and Treatments in Digestive Malignancy)

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14 pages, 1586 KiB

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Hepatoma-Derived Growth Factor: An Overview and Its Role as a Potential Therapeutic Target Molecule for Digestive Malignancies

by Hirayuki Enomoto, Hideji Nakamura, Hiroki Nishikawa, Shuhei Nishiguchi and Hiroko Iijima

Int. J. Mol. Sci. 2020, 21(12), 4216; https://doi.org/10.3390/ijms21124216 - 13 Jun 2020

Cited by 11 | Viewed by 2876

Abstract

Hepatoma-derived growth factor (HDGF) was identified in research seeking to find a novel growth factor for hepatoma cells. Subsequently, four HDGF-related proteins were identified, and these proteins are considered to be members of a new gene family. HDGF has a growth-stimulating role, an angiogenesis-inducing role, and a probable anti-apoptotic role. HDGF is ubiquitously expressed in non-cancerous tissues, and participates in organ development and in the healing of damaged tissues. In addition, the high expression of HDGF was reported to be closely associated with unfavorable clinical outcomes in several malignant diseases. Thus, HDGF is considered to contribute to the development and progression of malignant disease. We herein provide a brief overview of the factor and its functions in relation to benign and malignant cells. We also describe its possible role as a target molecule for digestive malignancies. Full article

(This article belongs to the Special Issue Molecular Mechanisms, Diagnosis and Treatments in Digestive Malignancy)

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23 pages, 1306 KiB

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TRP Channels in Digestive Tract Cancers

by Paulina Stokłosa, Anna Borgström, Sven Kappel and Christine Peinelt

Int. J. Mol. Sci. 2020, 21(5), 1877; https://doi.org/10.3390/ijms21051877 - 09 Mar 2020

Cited by 37 | Viewed by 6314

Abstract

Cancers of the digestive tract are among the most prevalent types of cancer. These types of cancers are often diagnosed at a late stage, which results in a poor prognosis. Currently, many biomedical studies focus on the role of ion channels, in particular transient receptor potential (TRP) channels, in cancer pathophysiology. TRP channels show mostly non-selective permeability to monovalent and divalent cations. TRP channels are often dysregulated in digestive tract cancers, which can result in alterations of cancer hallmark functions, such as enhanced proliferation, migration, invasion and the inability to induce apoptosis. Therefore, TRP channels could serve as potential diagnostic biomarkers. Moreover, TRP channels are mostly expressed on the cell surface and ion channel targeting drugs do not need to enter the cell, making them attractive candidate drug targets. In this review, we summarize the current knowledge about TRP channels in connection to digestive tract cancers (oral cancer, esophageal cancer, liver cancer, pancreatic cancer, gastric cancer and colorectal cancer) and give an outlook on the potential of TRP channels as cancer biomarkers or therapeutic targets. Full article

(This article belongs to the Special Issue Molecular Mechanisms, Diagnosis and Treatments in Digestive Malignancy)

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