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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 (28 February 2023) | Viewed by 16320

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Special Issue Editor

Prof. Dr. Guanbin Song

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Guest Editor

Key Laboratory of Biorheological Science and Technology, Ministry of Education, College of Bioengineering, Chongqing University, Chongqing 400030, China
Interests: stem cell biology; tumor biology; cancer therapy; tissue injury and repair; signal transduction; mechanobiology

Special Issue Information

Dear Colleagues,

Cancer is the leading cause of death worldwide, the management of the malignant tumor remains one of the most challenging problems in the clinic. Tumor microenvironment (TME) is a complex mixture comprised of cancer cells, stromal cells, immune cells, stem cells, tumor-associated fibroblasts (TAF), non-cellular components within extracellular matrix (ECM), et al., and plays a crucial role in tumorigenesis, growth, angiogenesis, invasion, metastasis and therapeutic efficacy of cancer. There are various factors affecting tumor cells in tumor microenvironment, including chemical factors, mechanical factors, biological factors and their coupling effects. Crosstalk between tumor cells and these factors is critical and contributes to tumor survival, progression, and metastasis, which involves complex signal transmission/transduction processes. Despite many efforts to elucidate crosstalk between cancer cells and tumor microenvironment, the signal pathways of these factors in cancer remain to be fully clarified.

In this special issue, we are seeking high-quality review articles, original research papers based on experiments in vitro or in vivo models or technical reports on the topic related to signal pathways in cancer. It should be noted that IJMS is a journal of molecular science, thus pure clinical studies will not suitable for this journal.

Dr. Guanbin Song
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

tumor cell/cancer cell
tumor stem cell/cancer stem cell
carcinogenesis
tumor microenvironment
tumor invasion/metastasis
differentidtion
signal pathway
mechanotransduction
cancer therapy
tumor metabolism
tumor immunology
tumor heterogeneity
molecular pathology

Published Papers (7 papers)

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Editorial

Jump to: Research, Review

3 pages, 171 KiB

Open AccessEditorial

Signal Pathways in Cancer

by Guanbin Song

Int. J. Mol. Sci. 2023, 24(9), 8260; https://doi.org/10.3390/ijms24098260 - 5 May 2023

Cited by 2 | Viewed by 1101

Abstract

Cancer is a major health-threatening disease and is the second leading cause of death worldwide; the prevention and treatment of cancer remains one of the most challenging problems clinically [...] Full article

(This article belongs to the Special Issue Signal Pathways in Cancer)

Research

Jump to: Editorial, Review

11 pages, 2593 KiB

Open AccessArticle

Plectin Downregulation Inhibits Migration and Suppresses Epithelial Mesenchymal Transformation of Hepatocellular Carcinoma Cells via ERK1/2 Signaling

by Rushuang Xu, Shan He, Di Ma, Rui Liang, Qing Luo and Guanbin Song

Int. J. Mol. Sci. 2023, 24(1), 73; https://doi.org/10.3390/ijms24010073 - 21 Dec 2022

Cited by 4 | Viewed by 1751

Abstract

Plectin, as a cytoskeleton-related protein, is involved in various physiological and pathological processes of many cell types. Studies have found that plectin affects cancer cell invasion and metastasis, but the exact mechanism is not fully understood. In this study, we aim to investigate the role of plectin in the migration of hepatocellular carcinoma (HCC) cells and explore its relevant molecular mechanism. Herein, we found that the expression of plectin in HCC tissue and cells was significantly increased compared with normal liver tissue and cells. After downregulation of plectin, the migration ability of HCC cells was significantly lower than that of the control group. Moreover, the expression of E-cadherin was upregulated and the expression of N-cadherin and vimentin was downregulated, suggesting that plectin downregulation suppresses epithelial mesenchymal transformation (EMT) of HCC cells. Mechanically, we found that plectin downregulation repressed the extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation. Activation of ERK1/2 recovered the plectin downregulation-inhibited migration and EMT of HCC cells. Taken together, our results demonstrate that downregulation of plectin inhibits HCC cell migration and EMT through ERK1/2 signaling, which provides a novel prognostic biomarker and potential therapeutic target for HCC. Full article

(This article belongs to the Special Issue Signal Pathways in Cancer)

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12 pages, 2858 KiB

Open AccessArticle

Nucleolar Stress Response via Ribosomal Protein L11 Regulates Topoisomerase Inhibitor Sensitivity of P53-Intact Cancers

by Yuka Ishihara, Kiyoshiro Nakamura, Shunsuke Nakagawa, Yasuhiro Okamoto, Masatatsu Yamamoto, Tatsuhiko Furukawa and Kohichi Kawahara

Int. J. Mol. Sci. 2022, 23(24), 15986; https://doi.org/10.3390/ijms232415986 - 15 Dec 2022

Cited by 3 | Viewed by 1513

Abstract

Nucleolar stress response is caused by perturbations in ribosome biogenesis, induced by the inhibition of ribosomal RNA processing and synthesis, as well as ribosome assembly. This response induces p53 stabilization and activation via ribosomal protein L11 (RPL11), suppressing tumor progression. However, anticancer agents that kill cells via this mechanism, and their relationship with the therapeutic efficiency of these agents, remain largely unknown. Here, we sought to investigate whether topoisomerase inhibitors can induce nucleolar stress response as they reportedly block ribosomal RNA transcription. Using rhabdomyosarcoma and rhabdoid tumor cell lines that are sensitive to the nucleolar stress response, we evaluated whether nucleolar stress response is associated with sensitivity to topoisomerase inhibitors ellipticine, doxorubicin, etoposide, topotecan, and anthracyclines. Cell proliferation assay indicated that small interfering RNA-mediated RPL11 depletion resulted in decreased sensitivity to topoisomerase inhibitors. Furthermore, the expression of p53 and its downstream target proteins via western blotting showed the suppression of p53 pathway activation upon RPL11 knockdown. These results suggest that the sensitivity of cancer cells to topoisomerase inhibitors is regulated by RPL11-mediated nucleolar stress responses. Thus, RPL11 expression may contribute to the prediction of the therapeutic efficacy of topoisomerase inhibitors and increase their therapeutic effect of topoisomerase inhibitors. Full article

(This article belongs to the Special Issue Signal Pathways in Cancer)

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23 pages, 38623 KiB

Open AccessArticle

The Novel Protein ADAMTS16 Promotes Gastric Carcinogenesis by Targeting IFI27 through the NF-κb Signaling Pathway

by Tuoyang Li, Junyi Zhou, Yingming Jiang, Yandong Zhao, Jintuan Huang, Weiyao Li, Zhenze Huang, Zijian Chen, Xiaocheng Tang, Hao Chen and Zuli Yang

Int. J. Mol. Sci. 2022, 23(19), 11022; https://doi.org/10.3390/ijms231911022 - 20 Sep 2022

Cited by 8 | Viewed by 2155

Abstract

A disintegrin and metalloproteinase with thrombospondin motifs 16 (ADAMTS16) has been reported to be involved in the pathogenesis of solid cancers. However, its role in gastric cancer (GC) is unclear. In this study, the role of ADAMTS16 in gastric cancer was investigated. The effects of ADAMTS16 on cell migration, invasion, and proliferation were investigated by functional experiments in vivo and in vitro. Downstream signal pathways of ADAMTS16 were confirmed by using bioinformatics analysis, co-immunoprecipitation, and immunofluorescence. Meanwhile, bioinformatics analysis, qRT-PCR, western blot, and dual-luciferase reporter gene analysis assays were used to identify ADAMTS16 targets. The expression of ADAMTS16 in GC was analyzed in public datasets. The expression of ADAMTS16 and its correlations with the clinical characteristics of GC were investigated by immunohistochemistry. Ectopic ADAMTS16 expression significantly promoted tumor cell migration, invasion, and growth. Bioinformatics analysis and western blot showed that ADAMTS16 upregulated the IFI27 protein through the NF-κb pathway, which was confirmed by immunofluorescence and western blot. Dual-luciferase reporter gene analysis identified a binding site between P65 and IFI27 that may be directly involved in the transcriptional regulation of IFI27. IFI27 knockdown reversed the promoting effect of ADAMTS16 on cell invasion, migration, and proliferation indicating that ADAMTS16 acts on GC cells by targeting the NF-κb/IFI27 axis. ADAMTS16 was associated with poor prognosis in clinical characteristics. ADAMTS16 promotes cell migration, invasion, and proliferation by targeting IFI27 through the NF-κB pathway and is a potential progressive and survival biomarker of GC. Full article

(This article belongs to the Special Issue Signal Pathways in Cancer)

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Review

Jump to: Editorial, Research

34 pages, 7763 KiB

Open AccessReview

Interplay between Signaling Pathways and Tumor Microenvironment Components: A Paradoxical Role in Colorectal Cancer

by Sonia Ben Hamouda and Khadija Essafi-Benkhadir

Int. J. Mol. Sci. 2023, 24(6), 5600; https://doi.org/10.3390/ijms24065600 - 15 Mar 2023

Cited by 5 | Viewed by 2699

Abstract

The study of the tumor microenvironment (TME) has become an important part of colorectal cancer (CRC) research. Indeed, it is now accepted that the invasive character of a primary CRC is determined not only by the genotype of the tumor cells, but also by their interactions with the extracellular environment, which thereby orchestrates the development of the tumor. In fact, the TME cells are a double-edged sword as they play both pro- and anti-tumor roles. The interaction of the tumor-infiltrating cells (TIC) with the cancer cells induces the polarization of the TIC, exhibiting an antagonist phenotype. This polarization is controlled by a plethora of interconnected pro- and anti-oncogenic signaling pathways. The complexity of this interaction and the dual function of these different actors contribute to the failure of CRC control. Thus, a better understanding of such mechanisms is of great interest and provides new opportunities for the development of personalized and efficient therapies for CRC. In this review, we summarize the signaling pathways linked to CRC and their implication in the development or inhibition of the tumor initiation and progression. In the second part, we enlist the major components of the TME and discuss the complexity of their cells functions. Full article

(This article belongs to the Special Issue Signal Pathways in Cancer)

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17 pages, 1131 KiB

Open AccessReview

Emerging Roles of Hedgehog Signaling in Cancer Immunity

by Alessandro Giammona, Enrica Crivaro and Barbara Stecca

Int. J. Mol. Sci. 2023, 24(2), 1321; https://doi.org/10.3390/ijms24021321 - 10 Jan 2023

Cited by 11 | Viewed by 3945

Abstract

Hedgehog–GLI (HH) signaling plays an essential role in embryogenesis and tissue homeostasis. Aberrant activation of the pathway through mutations or other mechanisms is involved in the development and progression of numerous types of cancer, including basal cell carcinoma, medulloblastoma, melanoma, breast, prostate, hepatocellular and pancreatic carcinomas. Activation of HH signaling sustains proliferation, suppresses cell death signals, enhances invasion and metastasis, deregulates cellular metabolism and promotes angiogenesis and tumor inflammation. Targeted inhibition of the HH pathway has therefore emerged as an attractive therapeutic strategy for the treatment of a wide range of cancers. Currently, the Smoothened (SMO) receptor and the downstream GLI transcriptional factors have been investigated for the development of targeted drugs. Recent studies have revealed that the HH signaling is also involved in tumor immune evasion and poor responses to cancer immunotherapy. Here we focus on the effects of HH signaling on the major cellular components of the adaptive and innate immune systems, and we present recent discoveries elucidating how the immunosuppressive function of the HH pathway is engaged by cancer cells to prevent immune surveillance. In addition, we discuss the future prospect of therapeutic options combining the HH pathway and immune checkpoint inhibitors. Full article

(This article belongs to the Special Issue Signal Pathways in Cancer)

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20 pages, 1076 KiB

Open AccessReview

Waldenström Macroglobulinemia: Mechanisms of Disease Progression and Current Therapies

by Ava J. Boutilier, Lina Huang and Sherine F. Elsawa

Int. J. Mol. Sci. 2022, 23(19), 11145; https://doi.org/10.3390/ijms231911145 - 22 Sep 2022

Cited by 4 | Viewed by 2281

Abstract

Waldenström macroglobulinemia is an indolent, B-cell lymphoma without a known cure. The bone marrow microenvironment and cytokines both play key roles in Waldenström macroglobulinemia (WM) tumor progression. Only one FDA-approved drug exists for the treatment of WM, Ibrutinib, but treatment plans involve a variety of drugs and inhibitors. This review explores avenues of tumor progression and targeted drug therapy that have been investigated in WM and related B-cell lymphomas. Full article

(This article belongs to the Special Issue Signal Pathways in Cancer)

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