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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 (31 October 2020) | Viewed by 15248

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Special Issue Editor

Prof. Dr. Keizo Kanasaki

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Internal Medicine 1, Shimane University Faculty of Medicine, 89-1 Enya-cho, Izumo, Shimane 693-8501, Japan
Interests: hyperglycemia; hyperinsulinemia and insulin resistance; obesity; diabetes
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Dear Colleagues,

Diabetes is a serious metabolic disease associate with multiple organ dysfunctions. The International Diabetes Federation reported that 425 million adults have diabetes, and 90% of them are type 2 diabetes. In addition to the classical vascular complications of diabetes, recent evidence suggests that diabetes could contribute to the onset, progression, and metastasis of certain cancers. Such effects on cancer biology in diabetic patients are complicated, since diabetes itself could affect cancer biology with hyperglycemia and hyperinsulinemia. Not only that, but obesity, the common comorbidity of type 2 diabetes, could influence them. Furthermore, diabetic drugs prescribed in the clinic play roles in cancer biology, and such effects of diabetic drugs must be analyzed and followed closely. Taken together, it is clear that intensive investigation is required in cancer biology in diabetes.

Therefore, in this Special Issue of IJMS, I am inviting original papers, commentaries to key papers, and review articles regarding cancer biology in diabetes.

Prof. Dr. Keizo Kanasaki
Guest Editor

Manuscript Submission Information

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Keywords

hyperglycemia
hyperinsulinemia and insulin resistance
obesity
glycolysis
extracellular matrix
oxidative stress
metastasis
inflammation
diabetic drug
metformin

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Published Papers (4 papers)

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Research

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14 pages, 7611 KiB

Open AccessArticle

Dictyostelium Differentiation-Inducing Factor-1 Promotes Glucose Uptake, at Least in Part, via an AMPK-Dependent Pathway in Mouse 3T3-L1 Cells

by Yuzuru Kubohara, Yoshimi Homma, Hiroshi Shibata, Yoshiteru Oshima and Haruhisa Kikuchi

Int. J. Mol. Sci. 2021, 22(5), 2293; https://doi.org/10.3390/ijms22052293 - 25 Feb 2021

Cited by 7 | Viewed by 2296

Abstract

Differentiation-inducing factor-1 (DIF-1) is a chlorinated alkylphenone (a polyketide) found in the cellular slime mold Dictyostelium discoideum. DIF-1 and its derivative, DIF-1(3M) promote glucose consumption in vitro in mammalian cells and in vivo in diabetic rats; they are expected to be the leading antiobesity and antidiabetes compounds. In this study, we investigated the mechanisms underlying the actions of DIF-1 and DIF-1(3M). In isolated mouse liver mitochondria, these compounds at 2–20 μM promoted oxygen consumption in a dose-dependent manner, suggesting that they act as mitochondrial uncouplers, whereas CP-DIF-1 (another derivative of DIF-1) at 10–20 μM had no effect. In confluent mouse 3T3-L1 fibroblasts, DIF-1 and DIF-1(3M) but not CP-DIF-1 induced phosphorylation (and therefore activation) of AMP kinase (AMPK) and promoted glucose consumption and metabolism. The DIF-induced glucose consumption was reduced by compound C (an AMPK inhibitor) or AMPK knock down. These data suggest that DIF-1 and DIF-1(3M) promote glucose uptake, at least in part, via an AMPK-dependent pathway in 3T3-L1 cells, whereas cellular metabolome analysis revealed that DIF-1 and DIF-1(3M) may act differently at least in part. Full article

(This article belongs to the Special Issue Cancer Biology in Diabetes)

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16 pages, 2852 KiB

Open AccessArticle

Alpha-Glucosidase Inhibitor Voglibose Suppresses Azoxymethane-Induced Colonic Preneoplastic Lesions in Diabetic and Obese Mice

by Junichi Kato, Yohei Shirakami, Taku Mizutani, Masaya Kubota, Hiroyasu Sakai, Takashi Ibuka and Masahito Shimizu

Int. J. Mol. Sci. 2020, 21(6), 2226; https://doi.org/10.3390/ijms21062226 - 23 Mar 2020

Cited by 8 | Viewed by 3402

Abstract

Type 2 diabetes mellitus and its related insulin resistance are known to increase the risk of cancer. Anti-diabetic agents can improve insulin resistance and may lead to the suppression of carcinogenesis. This study aimed to investigate the preventive effects of the alpha-glucosidase inhibitor voglibose on the development of azoxymethane-induced colorectal pre-neoplastic lesions in obese and diabetic C57BL/KsJ-db/db mice. The direct effects of voglibose on the proliferation of colorectal cancer cells were also evaluated. Mice were injected with azoxymethane to induce colorectal pre-malignancy and were then administered drinking water with or without voglibose. At the end of the study, the administration of voglibose significantly suppressed the development of colorectal neoplastic lesions. In voglibose-treated mice, serum glucose levels, oxidative stress, as well as mRNA expression of the insulin-like growth factor-1 in the colon mucosa, were reduced. The proliferation of human colorectal cancer cells was not altered by voglibose. These results suggested that voglibose suppressed colorectal carcinogenesis in a diabetes- and obesity-related colorectal cancer model, presumably by improving inflammation via the reduction of oxidative stress and suppressing of the insulin-like growth factor/insulin-like growth factor-1 receptor axis in the colonic mucosa. Full article

(This article belongs to the Special Issue Cancer Biology in Diabetes)

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13 pages, 3821 KiB

Open AccessArticle

Deficiency in Dipeptidyl Peptidase-4 Promotes Chemoresistance Through the CXCL12/CXCR4/mTOR/TGFβ Signaling Pathway in Breast Cancer Cells

by Shaolan Li, Yang Fan, Asako Kumagai, Emi Kawakita, Munehiro Kitada, Keizo Kanasaki and Daisuke Koya

Int. J. Mol. Sci. 2020, 21(3), 805; https://doi.org/10.3390/ijms21030805 - 26 Jan 2020

Cited by 22 | Viewed by 3811

Abstract

Dipeptidyl peptidase (DPP)-4, a molecular target of DPP-4 inhibitors, which are type 2 diabetes drugs, is expressed in a variety of cell types, tissues and organs. DPP-4 has been shown to be involved in cancer biology, and we have recently shown that a DPP-4 inhibitor promoted the epithelial mesenchymal transition (EMT) in breast cancer cells. The EMT is known to associate with chemotherapy resistance via the induction of ATP-binding cassette (ABC) transporters in cancer cells. Here, we demonstrated that deficiency in DPP-4 promoted chemotherapy resistance via the CXCL12/CXCR4/mTOR axis, activating the TGFβ signaling pathway via the expression of ABC transporters. DPP-4 inhibition enhanced ABC transporters in vivo and in vitro. Doxorubicin (DOX) further induced ABC transporters in DPP-4-deficient 4T1 cells, and the induction of ABC transporters was suppressed by either the CXCR4 inhibitor AMD3100, the mTOR inhibitor rapamycin or a neutralizing TGFβ (1, 2 and 3) antibody(N-TGFβ). Knockdown of snail, an EMT-inducible transcription factor, suppressed ABC transporter levels in DOX-treated DPP-4-deficient 4T1 cells. In an allograft mouse model, however, the effects of DOX in either primary tumor or metastasis were not statistically different between control and DPP-4-kd 4T1. Taken together, our findings suggest that DPP-4 inhibitors potentiate chemotherapy resistance via the induction of ABC transporters by the CXCL12/CXCR4/mTOR/TGFβ signaling pathway in breast cancer cells. Full article

(This article belongs to the Special Issue Cancer Biology in Diabetes)

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Review

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25 pages, 1479 KiB

Open AccessReview

Endometrial Cancer as a Metabolic Disease with Dysregulated PI3K Signaling: Shedding Light on Novel Therapeutic Strategies

by Satoru Kyo and Kentaro Nakayama

Int. J. Mol. Sci. 2020, 21(17), 6073; https://doi.org/10.3390/ijms21176073 - 23 Aug 2020

Cited by 22 | Viewed by 5356

Abstract

Endometrial cancer (EC) is one of the most common malignancies of the female reproductive organs. The most characteristic feature of EC is the frequent association with metabolic disorders. However, the components of these disorders that are involved in carcinogenesis remain unclear. Accumulating epidemiological studies have clearly revealed that hyperinsulinemia, which accompanies these disorders, plays central roles in the development of EC via the insulin-phosphoinositide 3 kinase (PI3K) signaling pathway as a metabolic driver. Recent comprehensive genomic analyses showed that over 90% of ECs have genomic alterations in this pathway, resulting in enhanced insulin signaling and production of optimal tumor microenvironments (TMEs). Targeting PI3K signaling is therefore an attractive treatment strategy. Several clinical trials for recurrent or advanced ECs have been attempted using PI3K-serine/threonine kinase (AKT) inhibitors. However, these agents exhibited far lower efficacy than expected, possibly due to activation of alternative pathways that compensate for the PIK3-AKT pathway and allow tumor growth, or due to adaptive mechanisms including the insulin feedback pathway that limits the efficacy of agents. Overcoming these responses with careful management of insulin levels is key to successful treatment. Further interest in specific TMEs via the insulin PI3K-pathway in obese women will provide insight into not only novel therapeutic strategies but also preventive strategies against EC. Full article

(This article belongs to the Special Issue Cancer Biology in Diabetes)

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