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Adhesion, Metastasis and Inhibition of Cancer Cells, 2nd Edition

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Biochemistry, Molecular and Cellular Biology".

Deadline for manuscript submissions: closed (31 December 2024) | Viewed by 6869

Special Issue Editor


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Guest Editor
Department of Pharmaceutical Sciences, College of Pharmacy, University of Michigan, 1600 Huron Pkwy, Ann Arbor, MI 48109, USA
Interests: drug resistance; metastasis; cancer drug development; toxicology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue aims to promote scientific understanding of cell–matrix adhesion and interactions between cancer cells and their surroundings which trigger metastasis and influence the evolution of malignant phenotypes such as drug resistance. Particularly welcome are short communications, review articles, original articles, and commentaries that focus on:

  • Cell-adhesion-mediated drug resistance and tumor metastasis;
  • The development of new therapeutic strategies to overcome metastasis or drug resistance by targeting new adhesion molecules in cancer treatments;
  • The development of new clinically relevant in vitro (microfluidics and lab-on-chip devices) and in vivo tumor metastasis models;
  • The discovery of new biomarkers (proteomic analysis and new gene mutations) involved in tumor metastasis and drug resistance;
  • Altered expressions of adhesion molecules with prognostic significance in cancer patients.

Dr. Zhongwei Liu
Guest Editor

Manuscript Submission Information

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Keywords

  • adhesion molecules
  • epithelial–mesenchymal transition (EMT)
  • tumor microenvironment (TME)
  • metastasis
  • drug resistance
  • biomarkers
  • extracellular matrix (ECM)
  • microfluidics
  • epidemiology

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Published Papers (5 papers)

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Research

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9 pages, 1960 KiB  
Article
Epidermal Growth Factor Downregulates Carbon Anhydrase III (CAIII) in Colon Cancer
by Derya Okuyan
Curr. Issues Mol. Biol. 2024, 46(11), 12994-13002; https://doi.org/10.3390/cimb46110774 - 14 Nov 2024
Viewed by 935
Abstract
Colorectal cancer (CRC) is the second leading cause of cancer-related death in the world. Dysregulations in the EGF signaling pathway have been associated with colon cancer. Some members of the carbonic anhydrase family serve as biomarkers in cancer. Carbonic anhydrase III (CAIII), a [...] Read more.
Colorectal cancer (CRC) is the second leading cause of cancer-related death in the world. Dysregulations in the EGF signaling pathway have been associated with colon cancer. Some members of the carbonic anhydrase family serve as biomarkers in cancer. Carbonic anhydrase III (CAIII), a member of this family, shows different activities than the other members of its family and has been associated with cancer. However, there are no studies on the effective regulation of EGF. In this study, we investigated the EGF-influenced regulation of CAIII in the HT29, SW480, and HUVEC cell lines and showed that CAIII regulation decreased with the effect of EGF. We aimed to investigate the EGF-affected mRNA and protein regulation of the CAIII gene in HT29, SW480, and HUVEC cell lines. For this purpose, we determined time-dependent CAIII mRNA and protein expression by applying EGF to HT29, SW480, and HUVEC cells. Time-dependent EGF-induced mRNA and protein level regulation of the CAIII gene decreased in the HT29, SW480, and HUVEC cell lines. EGF regulates the motility, adhesion, and metastasis of cancer cells. CAIII prevents cells from metastasizing through cell acidification. Therefore, our findings explained why the EGF-effective regulation of CAIII decreased. We suggest that the CAIII gene is promising as a targeted therapy due to the decrease in EGF-effected CAIII gene regulation in colon carcinoma. Full article
(This article belongs to the Special Issue Adhesion, Metastasis and Inhibition of Cancer Cells, 2nd Edition)
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13 pages, 3255 KiB  
Article
Switch/Sucrose Non-Fermentable (SWI/SNF) Complex—Partial Loss in Sinonasal Squamous Cell Carcinoma: A High-Grade Morphology Impact and Progression
by Roberto Onner Cruz-Tapia, Ana María Cano-Valdez, Abelardo Meneses-García, Lorena Correa-Arzate, Adriana Molotla-Fragoso, Guillermo Villagómez-Olea, Diana Brisa Sevilla-Lizcano and Javier Portilla-Robertson
Curr. Issues Mol. Biol. 2024, 46(11), 12183-12195; https://doi.org/10.3390/cimb46110723 - 30 Oct 2024
Viewed by 994
Abstract
Sinonasal carcinomas are aggressive neoplasms that present a high morbidity and mortality rate with an unfavorable prognosis. This group of tumors exhibits morphological and genetic diversity. Genetic and epigenetic alterations in these neoplasms are the current targets for diagnosis and treatment. The most [...] Read more.
Sinonasal carcinomas are aggressive neoplasms that present a high morbidity and mortality rate with an unfavorable prognosis. This group of tumors exhibits morphological and genetic diversity. Genetic and epigenetic alterations in these neoplasms are the current targets for diagnosis and treatment. The most common type of cancer originating in the sinonasal tract is sinonasal squamous cell carcinomas (SNSCCs), which present different histological patterns and variable histological aggressiveness. A significant number of alterations have been reported in sinonasal tumors, including deficiencies in the Switch/Sucrose non-fermentable (SWI/SNF) chromatin remodeling complex. In the sinonasal tract, deficiencies of the subunits SMARCB1/INI1, SMARCA4/BRG1, and SMARCA2 have been noted in carcinomas, adenocarcinomas, and soft tissue tumors with a distinctive high-grade morphology and a fatal prognosis. Objective: The objective of this study is to identify the status of the SWI/SNF complex using immunohistochemistry in sinonasal squamous cell carcinomas and their association with morphology and survival. Methods: A total of 103 sinonasal carcinomas with different grades of squamous differentiation were analyzed; the selection was based on those cases with high-grade morphology. The carcinomas were then evaluated immunohistochemically for SMARCB1 and SMARCA4 proteins. Their expression was compared with the biological behavior and survival of the patients. Results: Among the SNSCCs, 47% corresponded to the non-keratinizing squamous cell carcinoma (NKSCC) type with high-grade characteristics, 40% were keratinizing squamous cell carcinomas (KSCCs), 9% were SMARCB1-deficient carcinomas, and 4% were SMARCA4-deficient carcinomas. Mosaic expression for SMARCB1 (NKSCC—33%; KSCC—21.9%) and SMARCA4 (NKSCC—14.6%; KSCC—12.2%) was identified, showing an impact on tumor size and progression. Conclusions: We identified that that the partial loss (mosaic expression) of SMARCB1 in SNSCCs is associated with high-grade malignant characteristics and a negative effect on patient survival; meanwhile, SMARCA4-mosaic expression in SNSCCs is associated with high-grade malignant characteristics and an increase in tumor size concerning the intact SMARCA4. Full article
(This article belongs to the Special Issue Adhesion, Metastasis and Inhibition of Cancer Cells, 2nd Edition)
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13 pages, 3975 KiB  
Article
Isocorydine Exerts Anticancer Activity by Disrupting the Energy Metabolism and Filamentous Actin Structures of Oral Squamous Carcinoma Cells
by Qiaozhen Zhou, Qianqian Zhang, Lingzi Liao, Qian Li, Huidan Qu, Xinyu Wang, Ying Zhou, Guangzeng Zhang, Mingliang Sun, Kailiang Zhang and Baoping Zhang
Curr. Issues Mol. Biol. 2024, 46(1), 650-662; https://doi.org/10.3390/cimb46010042 - 9 Jan 2024
Cited by 1 | Viewed by 1685
Abstract
Isocorydine (ICD) exhibits strong antitumor effects on numerous human cell lines. However, the anticancer activity of ICD against oral squamous cell carcinoma (OSCC) has not been reported. The anticancer activity, migration and invasion ability, and changes in the cytoskeleton morphology and mechanical properties [...] Read more.
Isocorydine (ICD) exhibits strong antitumor effects on numerous human cell lines. However, the anticancer activity of ICD against oral squamous cell carcinoma (OSCC) has not been reported. The anticancer activity, migration and invasion ability, and changes in the cytoskeleton morphology and mechanical properties of ICD in OSCC were determined. Changes in the contents of reactive oxygen species (ROS), the mitochondrial membrane potential (MMP), ATP, and mitochondrial respiratory chain complex enzymes Ⅰ–Ⅳ in cancer cells were studied. ICD significantly inhibited the proliferation of oral tongue squamous cells (Cal-27), with an IC50 of 0.61 mM after 24 h of treatment. The invasion, migration, and adhesion of cancer cells were decreased, and cytoskeletal actin was deformed and depolymerized. In comparison to an untreated group, the activities of mitochondrial respiratory chain complex enzymes I-IV were significantly decreased by 50.72%, 27.39%, 77.27%, and 73.89%, respectively. The ROS production increased, the MMP decreased by 43.65%, and the ATP content decreased to 17.1 ± 0.001 (mmol/mL); ultimately, the apoptosis rate of cancer cells increased up to 10.57% after 24 h of action. These findings suggest that ICD exerted an obvious anticancer activity against OSCC and may inhibit Cal-27 proliferation and growth by causing mitochondrial dysfunction and interrupting cellular energy. Full article
(This article belongs to the Special Issue Adhesion, Metastasis and Inhibition of Cancer Cells, 2nd Edition)
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Review

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19 pages, 1559 KiB  
Review
Chimeric Antigen Receptor Cell Therapy: Empowering Treatment Strategies for Solid Tumors
by Tang-Her Jaing, Yi-Wen Hsiao and Yi-Lun Wang
Curr. Issues Mol. Biol. 2025, 47(2), 90; https://doi.org/10.3390/cimb47020090 - 31 Jan 2025
Viewed by 324
Abstract
Chimeric antigen receptor-T (CAR-T) cell therapy has demonstrated impressive efficacy in the treatment of blood cancers; however, its effectiveness against solid tumors has been significantly limited. The differences arise from a range of difficulties linked to solid tumors, including an unfriendly tumor microenvironment, [...] Read more.
Chimeric antigen receptor-T (CAR-T) cell therapy has demonstrated impressive efficacy in the treatment of blood cancers; however, its effectiveness against solid tumors has been significantly limited. The differences arise from a range of difficulties linked to solid tumors, including an unfriendly tumor microenvironment, variability within the tumors, and barriers to CAR-T cell infiltration and longevity at the tumor location. Research shows that the reasons for the decreased effectiveness of CAR-T cells in treating solid tumors are not well understood, highlighting the ongoing need for strategies to address these challenges. Current strategies frequently incorporate combinatorial therapies designed to boost CAR-T cell functionality and enhance their capacity to effectively target solid tumors. However, these strategies remain in the testing phase and necessitate additional validation to assess their potential benefits. CAR-NK (natural killer), CAR-iNKT (invariant natural killer T), and CAR-M (macrophage) cell therapies are emerging as promising strategies for the treatment of solid tumors. Recent studies highlight the construction and optimization of CAR-NK cells, emphasizing their potential to overcome the unique challenges posed by the solid tumor microenvironment, such as hypoxia and metabolic barriers. This review focuses on CAR cell therapy in the treatment of solid tumors. Full article
(This article belongs to the Special Issue Adhesion, Metastasis and Inhibition of Cancer Cells, 2nd Edition)
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16 pages, 698 KiB  
Review
Role of Filamin A in Growth and Migration of Breast Cancer—Review
by Patryk Zawadka, Wioletta Zielińska, Maciej Gagat and Magdalena Izdebska
Curr. Issues Mol. Biol. 2024, 46(4), 3408-3423; https://doi.org/10.3390/cimb46040214 - 17 Apr 2024
Cited by 1 | Viewed by 2261
Abstract
Despite ongoing research in the field of breast cancer, the morbidity rates indicate that the disease remains a significant challenge. While patients with primary tumors have relatively high survival rates, these chances significantly decrease once metastasis begins. Thus, exploring alternative approaches, such as [...] Read more.
Despite ongoing research in the field of breast cancer, the morbidity rates indicate that the disease remains a significant challenge. While patients with primary tumors have relatively high survival rates, these chances significantly decrease once metastasis begins. Thus, exploring alternative approaches, such as targeting proteins overexpressed in malignancies, remains significant. Filamin A (FLNa), an actin-binding protein (ABP), is involved in various cellular processes, including cell migration, adhesion, proliferation, and DNA repair. Overexpression of the protein was confirmed in samples from patients with numerous oncological diseases such as prostate, lung, gastric, colorectal, and pancreatic cancer, as well as breast cancer. Although most researchers concur on its role in promoting breast cancer progression and aggressiveness, discrepancies exist among studies. Moreover, the precise mechanisms through which FLNa affects cell migration, invasion, and even cancer progression remain unclear, highlighting the need for further research. To evaluate FLNa’s potential as a therapeutic target, we have summarized its roles in breast cancer. Full article
(This article belongs to the Special Issue Adhesion, Metastasis and Inhibition of Cancer Cells, 2nd Edition)
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