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Novel Therapeutic Targets and Approaches, Genetic Markers and Signaling Pathways...
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Novel Therapeutic Targets and Approaches, Genetic Markers and Signaling Pathways in Neoplasms

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell and Gene Therapy".

Deadline for manuscript submissions: 15 May 2025 | Viewed by 17559

Special Issue Editors

Dr. Daria A. Chudakova

E-Mail Website
Guest Editor
Federal Center of Brain Research and Neurotechnologies of the Federal Medical Biological Agency, Moscow, Russia
Interests: cancer biology; ageing; cell fate, reprogramming and regeneration; epigenetics
Dr. Kazuyuki Kitatani

E-Mail Website
Guest Editor
Laboratory of Immunopharmacology, Faculty of Pharmaceutical Sciences, Setsunan University, Hirakata 573‐0101, Japan
Interests: sphingolipids; ceramides; sphingotherapy; cancer therapy; cancer biology; cancer metastasis; cellular signaling; cell death; necroptosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The study of human neoplastic diseases is a burgeoning and blazing-hot area of biomedicine. However, despite significant advances in this field, some patients are misdiagnosed and, for some, no effective treatments currently available. This Special Issue will provide an overview on the emerging therapeutic targets, approaches and molecular tools as well as novel genetic markers and signaling pathways in neoplasms (benign, malignant and of uncertain or unknown behavior). We welcome pioneering research-based works looking at the subject from a new angle. We also encourage the authors to present their review articles and formulate principally novel views on a subject, as long as their hypothesis and opinions are strongly supported by the body of the previously published experimental data. Research with direct clinical and translational application opening novel curative and diagnostic options is of particular interest.

Dr. Daria A. Chudakova
Dr. Kazuyuki Kitatani
Guest Editors

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 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

  • cancer
  • neoplasms
  • personalized medicine
  • genetic markers
  • next-generation sequencing (NGS)
  • whole-genome sequencing
  • signaling pathways in cancer
  • novel therapeutic targets
  • drug development

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Published Papers (10 papers)

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Research

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16 pages, 5322 KiB  
Article
Gene–Environment Interaction: Small Deletions (DELs) and Transcriptomic Profiles in Non-Melanoma Skin Cancer (NMSC) and Potential Implications for Therapy
by Farzana Jasmine, Armando Almazan, Yuliia Khamkevych, Maria Argos, Mohammad Shahriar, Tariqul Islam, Christopher R. Shea, Habibul Ahsan and Muhammad G. Kibriya
Cells 2025, 14(2), 95; https://doi.org/10.3390/cells14020095 - 10 Jan 2025
Viewed by 611
Abstract
Arsenic (As) is a risk factor for non-melanoma skin cancer (NMSC). From a six-year follow-up study on 7000 adults exposed to As, we reported the associations of single-nucleotide variation in tumor tissue and gene expression. Here, we identify the associations of small deletions [...] Read more.
Arsenic (As) is a risk factor for non-melanoma skin cancer (NMSC). From a six-year follow-up study on 7000 adults exposed to As, we reported the associations of single-nucleotide variation in tumor tissue and gene expression. Here, we identify the associations of small deletions (DELs) and transcriptomic profiles in NMSC. Comparing the (a) NMSC tissue (n = 32) and corresponding blood samples from each patient, and (b) an independent set of non-lesional, healthy skin (n = 16) and paired blood, we identified NMSC-associated DELs. Differential expressions of certain gene pathways (TGF-β signaling pathway, IL-17 pathway, PD-L1 pathway, etc.) showed significant interactions with these somatic DELs and As exposure. In low-As-exposure cases, the DELs in APC were associated with the up-regulation of inflamed T-Cell-associated genes by a fold change (FC) of 8.9 (95% CI 4.5–17.6), compared to 5.7 (95% CI 2.9–10.8) without APC DELs; in high-As-exposure cases, the APC DELs were associated with an FC of 5.8 (95% CI 3.5–9.8) compared to 1.2 (95% CI −1.3 to 1.8) without APC DELs. We report, for the first time, the significant associations of somatic DELs (many in STR regions) in NMSC tissue and As exposure with many dysregulated gene pathways. These findings may help in selecting groups of patients for potential targeted therapy like PD-L1 inhibitors, IL-17 inhibitors, and TGF-β inhibitors in the future. Full article
(This article belongs to the Special Issue Novel Therapeutic Targets and Approaches, Genetic Markers and Signaling Pathways in Neoplasms)
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22 pages, 5560 KiB  
Article
Myeloid Cell Mobilization and Recruitment by Human Mesothelioma in NSG-SGM3 Mice
by Vadim V. Shindyapin, Ekaterina O. Gubernatorova, Ekaterina A. Gorshkova, Nelya R. Chicherina, Fedor A. Sysonov, Anastasia S. Yakovleva, Daria A. Bogdanova, Oleg N. Demidov, Mariya V. Samsonova, Vladimir P. Baklaushev, Gaukhar M. Yusubalieva and Marina S. Drutskaya
Cells 2024, 13(24), 2135; https://doi.org/10.3390/cells13242135 - 23 Dec 2024
Viewed by 641
Abstract
Malignant pleural mesothelioma is a neoplasm that is often detected late due to nonspecific symptoms. This study utilized NSG-SGM3 mice to examine interactions between a human-derived mesothelioma reporter cell line (MZT-Luc2-mCherry) and the host’s myeloid compartment. Tumor growth was assessed using optical tomography, [...] Read more.
Malignant pleural mesothelioma is a neoplasm that is often detected late due to nonspecific symptoms. This study utilized NSG-SGM3 mice to examine interactions between a human-derived mesothelioma reporter cell line (MZT-Luc2-mCherry) and the host’s myeloid compartment. Tumor growth was assessed using optical tomography, while cytokine/chemokine production was analyzed via multiplex assay. Histological and immunohistochemical analyses validated the epithelioid mesothelioma phenotype. In vitro mesothelioma cells secreted factors associated with myeloid cell chemoattraction and functions supporting the previously reported myeloid-biased secretory phenotype. In line with this, post-engraftment analysis revealed increased neutrophil-like Ly6G+ populations and decreased Ly6C+ inflammatory monocytes in the blood of tumor-bearing mice. Significant Ly6G+ cell infiltration was observed in the tumor, while CD11b+ myeloid cells were localized primarily in the tumor periphery. Tumor lysates showed increased levels of neutrophil chemoattractants and G-CSF, suggesting a previously not reported role of neutrophils in mesothelioma progression. This novel model provides a platform for studying mesothelioma–host interactions, focusing on the myeloid compartment. It may also serve as a tool to facilitate the development of new therapeutic strategies targeting myeloid cell-mediated mechanisms in mesothelioma. Full article
(This article belongs to the Special Issue Novel Therapeutic Targets and Approaches, Genetic Markers and Signaling Pathways in Neoplasms)
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17 pages, 6263 KiB  
Article
Polo-like Kinase 1 Predicts Lymph Node Metastasis in Middle Eastern Colorectal Cancer Patients; Its Inhibition Reverses 5-Fu Resistance in Colorectal Cancer Cells
by Pratheesh Kumar Poyil, Abdul K. Siraj, Divya Padmaja, Sandeep Kumar Parvathareddy, Khadija Alobaisi, Saravanan Thangavel, Rafia Begum, Roxanne Diaz, Fouad Al-Dayel and Khawla S. Al-Kuraya
Cells 2024, 13(20), 1700; https://doi.org/10.3390/cells13201700 - 14 Oct 2024
Cited by 1 | Viewed by 1037
Abstract
Polo-like kinase 1 (PLK1) is a serine/threonine–protein kinase essential for regulating multiple stages of cell cycle progression in mammals. Aberrant regulation of PLK1 has been observed in numerous human cancers and is linked to poor prognoses. However, its role in the pathogenesis of [...] Read more.
Polo-like kinase 1 (PLK1) is a serine/threonine–protein kinase essential for regulating multiple stages of cell cycle progression in mammals. Aberrant regulation of PLK1 has been observed in numerous human cancers and is linked to poor prognoses. However, its role in the pathogenesis of colorectal cancer (CRC) in the Middle East remains unexplored. PLK1 overexpression was noted in 60.3% (693/1149) of CRC cases and was significantly associated with aggressive clinico-pathological parameters and p-ERK1/2 overexpression. Intriguingly, multivariate logistic regression analysis identified PLK1 as an independent predictor of lymph node metastasis. Our in vitro experiments demonstrated that CRC cells with high PLK1 levels were resistant to 5-Fu treatment, while those with low PLK1 expression were sensitive. To investigate PLK1′s role in chemoresistance, we used the specific inhibitor volasertib, which effectively reversed 5-Fu resistance. Interestingly, forced PLK1 expression activated the CRAF-MEK-ERK signaling cascade, while its inhibition suppressed this cascade. PLK1 knockdown reduced epithelial-to-mesenchymal transition (EMT) progression and stem cell-like traits in 5-Fu-resistant cells, implicating PLK1 in EMT induction and stemness in CRC. Moreover, silencing ERK1/2 significantly mitigated chemoresistance, EMT, and stemness properties in CRC cell lines that express PLK1. Furthermore, the knockdown of Zeb1 attenuated EMT and stemness, suggesting a possible link between EMT activation and the maintenance of stemness in CRC. Our findings underscore the pivotal role of PLK1 in mediating chemoresistance and suggest that PLK1 inhibition may represent a potential therapeutic strategy for the management of aggressive colorectal cancer subtypes. Full article
(This article belongs to the Special Issue Novel Therapeutic Targets and Approaches, Genetic Markers and Signaling Pathways in Neoplasms)
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19 pages, 9808 KiB  
Article
Decorin (DCN) Downregulation Activates Breast Stromal Fibroblasts and Promotes Their Pro-Carcinogenic Effects through the IL-6/STAT3/AUF1 Signaling
by Wafaa A. Aljagthmi, Manal A. Alasmari, Maha H. Daghestani, Layla A. Al-Kharashi, Falah H. Al-Mohanna and Abdelilah Aboussekhra
Cells 2024, 13(8), 680; https://doi.org/10.3390/cells13080680 - 14 Apr 2024
Cited by 1 | Viewed by 2868
Abstract
Decorin (DCN), a member of the small leucine-rich proteoglycan gene family, is secreted from stromal fibroblasts with non-cell-autonomous anti-breast-cancer effects. Therefore, in the present study, we sought to elucidate the function of decorin in breast stromal fibroblasts (BSFs). We first showed DCN downregulation [...] Read more.
Decorin (DCN), a member of the small leucine-rich proteoglycan gene family, is secreted from stromal fibroblasts with non-cell-autonomous anti-breast-cancer effects. Therefore, in the present study, we sought to elucidate the function of decorin in breast stromal fibroblasts (BSFs). We first showed DCN downregulation in active cancer-associated fibroblasts (CAFs) compared to their adjacent tumor counterpart fibroblasts at both the mRNA and protein levels. Interestingly, breast cancer cells and the recombinant IL-6 protein, both known to activate fibroblasts in vitro, downregulated DCN in BSFs. Moreover, specific DCN knockdown in breast fibroblasts modulated the expression/secretion of several CAF biomarkers and cancer-promoting proteins (α-SMA, FAP- α, SDF-1 and IL-6) and enhanced the invasion/proliferation abilities of these cells through activation of the STAT3/AUF1 signaling. Furthermore, DCN-deficient fibroblasts promoted the epithelial-to-mesenchymal transition and stemness processes in BC cells in a paracrine manner, which increased their resistance to cisplatin. These DCN-deficient fibroblasts also enhanced angiogenesis and orthotopic tumor growth in mice in a paracrine manner. On the other hand, ectopic expression of DCN in CAFs suppressed their active features and their paracrine pro-carcinogenic effects. Together, the present findings indicate that endogenous DCN suppresses the pro-carcinogenic and pro-metastatic effects of breast stromal fibroblasts. Full article
(This article belongs to the Special Issue Novel Therapeutic Targets and Approaches, Genetic Markers and Signaling Pathways in Neoplasms)
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18 pages, 19121 KiB  
Article
Analysis of the Expression of LSF Transcription Factor in the Regulation of Transcription and TSG101 during the Neoplastic Transformation of Endometrial Cells
by Rafał Ziemiński, Aleksandra Stupak, Maciej Kwiatek, Tomasz Gęca, Alicja Warowicka, Karolina Hejne, Anna Kwaśniewska, Anna Goździcka-Józefiak and Wojciech Kwaśniewski
Cells 2024, 13(7), 580; https://doi.org/10.3390/cells13070580 - 26 Mar 2024
Viewed by 1216
Abstract
Previous research indicates that carcinogenesis involves disrupting the functions of numerous genes, including factors involved in the regulation of transcription and cell proliferation. For these reasons, in endometrial carcinogenesis, we decided to investigate the expression of TSG101 (a suppressor of tumor transformation) and [...] Read more.
Previous research indicates that carcinogenesis involves disrupting the functions of numerous genes, including factors involved in the regulation of transcription and cell proliferation. For these reasons, in endometrial carcinogenesis, we decided to investigate the expression of TSG101 (a suppressor of tumor transformation) and LSF (a transcription factor involved in numerous cellular processes, such as cell cycle regulation, cell growth, development, and apoptosis). LSF may be involved in the regulation of TSG101 expression. The research material consisted of endometrial cancer samples from 60 patients. The control group consisted of normal endometrium samples donated by 60 women undergoing surgery for benign diseases of the female reproductive organs. The samples were subjected to immunohistochemical staining with antibodies specific to TSG101 and LSF. Specific antibodies were used to identify TSG101 and LSF in the examined histopathological preparations. An approximately 14-fold lower risk of endometrial cancer development was observed in patients with TSG expression in more than 75% of the assessed cells (4% vs. 36%; OR = 0.07; p = 0.0182). There was a four-fold lower risk of endometrial cancer development in patients with LSF expression in more than 50% of the assessed cells (32% vs. 64%; OR = 0.26; p = 0.0262). A more than three-fold lower risk of endometrial cancer development was observed in patients with LSF expression in more than 75% of the assessed cells (24% vs. 52%; OR = 0.29; p = 0.0454). Endometrial cancer was diagnosed in those with a lower level of TSG101 expression than in those with a cancer-free endometrium. Decreased expression of TSG101 may be a marker of endometrial cancer, and increased expression of LSF when diagnosed with endometrial cancer may indicate greater advancement of the disease. These markers might be used as diagnostic and prognostic markers—however, there is a lack of a correlation between them. Full article
(This article belongs to the Special Issue Novel Therapeutic Targets and Approaches, Genetic Markers and Signaling Pathways in Neoplasms)
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12 pages, 3459 KiB  
Article
Pronecroptotic Therapy Using Ceramide Nanoliposomes Is Effective for Triple-Negative Breast Cancer Cells
by Yuki Ohya, Yuri Ogiso, Masaya Matsuda, Harumi Sakae, Kentaro Nishida, Yasuhiro Miki, Todd E. Fox, Mark Kester, Wataru Sakamoto, Takeshi Nabe and Kazuyuki Kitatani
Cells 2024, 13(5), 405; https://doi.org/10.3390/cells13050405 - 26 Feb 2024
Cited by 2 | Viewed by 1814
Abstract
Regulated necrosis, termed necroptosis, represents a potential therapeutic target for refractory cancer. Ceramide nanoliposomes (CNLs), considered potential chemotherapeutic agents, induce necroptosis by targeting the activating protein mixed lineage kinase domain-like protein (MLKL). In the present study, we examined the potential of pronecroptotic therapy [...] Read more.
Regulated necrosis, termed necroptosis, represents a potential therapeutic target for refractory cancer. Ceramide nanoliposomes (CNLs), considered potential chemotherapeutic agents, induce necroptosis by targeting the activating protein mixed lineage kinase domain-like protein (MLKL). In the present study, we examined the potential of pronecroptotic therapy using CNLs for refractory triple-negative breast cancer (TNBC), for which there is a lack of definite and effective therapeutic targets among the various immunohistological subtypes of breast cancer. MLKL mRNA expression in tumor tissues was significantly higher in TNBC patients than in those with non-TNBC subtypes. Similarly, among the 50 breast cancer cell lines examined, MLKL expression was higher in TNBC-classified cell lines. TNBC cell lines were more susceptible to the therapeutic effects of CNLs than the non-TNBC subtypes of breast cancer cell lines. In TNBC-classified MDA-MB-231 cells, the knockdown of MLKL suppressed cell death induced by CNLs or the active substance short-chain C6-ceramide. Accordingly, TNBC cells were prone to CNL-evoked necroptotic cell death. These results will contribute to the development of CNL-based pronecroptotic therapy for TNBC. Full article
(This article belongs to the Special Issue Novel Therapeutic Targets and Approaches, Genetic Markers and Signaling Pathways in Neoplasms)
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Review

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17 pages, 3518 KiB  
Review
Small Molecule with Big Impact: Metarrestin Targets the Perinucleolar Compartment in Cancer Metastasis
by Vivek K. Kashyap, Bhuvnesh P. Sharma, Divya Pandey, Ajay K. Singh, Godwin Peasah-Darkwah, Bhupesh Singh, Kuldeep K. Roy, Murali M. Yallapu and Subhash C. Chauhan
Cells 2024, 13(24), 2053; https://doi.org/10.3390/cells13242053 - 12 Dec 2024
Viewed by 1026
Abstract
Metarrestin (ML246) is a first-in-class pyrrole–pyrimidine-derived small molecule that selectively targets the perinucleolar compartment (PNC). PNC is a distinct subnuclear structure predominantly found in solid tumor cells. The occurrence of PNC demonstrates a positive correlation with malignancy, serving as an indicator of tumor [...] Read more.
Metarrestin (ML246) is a first-in-class pyrrole–pyrimidine-derived small molecule that selectively targets the perinucleolar compartment (PNC). PNC is a distinct subnuclear structure predominantly found in solid tumor cells. The occurrence of PNC demonstrates a positive correlation with malignancy, serving as an indicator of tumor aggressiveness, progression, and metastasis. Various promising preclinical results have led to the clinical translation of metarrestin into a first-in-human trial. This review aims to summarize (i) the current understanding of the structure and function of PNC and its role in cancer progression and metastasis, (ii) key findings from studies examining the effect of metarrestin on various cancers across the translational spectrum, including in vitro, in vivo, and human clinical trial studies, and (iii) the pharmaceutical relevance of metarrestin as a promising anticancer candidate. Furthermore, our molecular docking and MD simulation studies show that metarrestin binds to eEF1A1 and eEF1A2 with a strong and stable affinity and inhibits eEF1A2 more efficiently compared to eEF1A1. The promising results from preclinical studies suggest that metarrestin has the potential to revolutionize the treatment of cancer, heralding a paradigm shift in its therapeutic management. Full article
(This article belongs to the Special Issue Novel Therapeutic Targets and Approaches, Genetic Markers and Signaling Pathways in Neoplasms)
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13 pages, 279 KiB  
Review
Genetic and Molecular Heterogeneity of Synovial Sarcoma and Associated Challenges in Therapy
by Ekaterina A. Lesovaya, Timur I. Fetisov, Beniamin Yu. Bokhyan, Varvara P. Maksimova, Evgeny P. Kulikov, Gennady A. Belitsky, Kirill I. Kirsanov and Marianna G. Yakubovskaya
Cells 2024, 13(20), 1695; https://doi.org/10.3390/cells13201695 - 14 Oct 2024
Viewed by 1823
Abstract
Synovial sarcoma (SS) is one of the most common types of pediatric soft tissue sarcoma (STS) being far less frequent in adults. This STS type is characterized by one specific chromosomal translocation SS18-SSX and the associated changes in signaling. However, other genetic and [...] Read more.
Synovial sarcoma (SS) is one of the most common types of pediatric soft tissue sarcoma (STS) being far less frequent in adults. This STS type is characterized by one specific chromosomal translocation SS18-SSX and the associated changes in signaling. However, other genetic and epigenetic abnormalities in SS do not necessarily include SS18-SSX-related events, but abnormalities are more sporadic and do not correlate well with the prognosis and response to therapy. Currently, targeted therapy for synovial sarcoma includes a limited range of drugs, and surgical resection is the mainstay treatment for localized cancer with adjuvant or neoadjuvant chemotherapy and radiotherapy. Understanding the molecular characteristics of synovial sarcoma subtypes is becoming increasingly important for detecting new potential targets and developing innovative therapies. Novel approaches to treating synovial sarcoma include immune-based therapies (such as TCR-T cell therapy to NY-ESO-1, MAGE4, PRAME or using immune checkpoint inhibitors), epigenetic modifiers (HDAC inhibitors, EZH2 inhibitors, BRD disruptors), as well as novel or repurposed receptor tyrosine kinase inhibitors. In the presented review, we aimed to summarize the genetic and epigenetic landscape of SS as well as to find out the potential niches for the development of novel diagnostics and therapies. Full article
(This article belongs to the Special Issue Novel Therapeutic Targets and Approaches, Genetic Markers and Signaling Pathways in Neoplasms)
39 pages, 2256 KiB  
Review
Tumor-Agnostic Therapy—The Final Step Forward in the Cure for Human Neoplasms?
by Mohamed Mahmoud El-Sayed, Julia Raffaella Bianco, YiJing Li and Zsolt Fabian
Cells 2024, 13(12), 1071; https://doi.org/10.3390/cells13121071 - 20 Jun 2024
Viewed by 1616
Abstract
Cancer accounted for 10 million deaths in 2020, nearly one in every six deaths annually. Despite advancements, the contemporary clinical management of human neoplasms faces a number of challenges. Surgical removal of tumor tissues is often not possible technically, while radiation and chemotherapy [...] Read more.
Cancer accounted for 10 million deaths in 2020, nearly one in every six deaths annually. Despite advancements, the contemporary clinical management of human neoplasms faces a number of challenges. Surgical removal of tumor tissues is often not possible technically, while radiation and chemotherapy pose the risk of damaging healthy cells, tissues, and organs, presenting complex clinical challenges. These require a paradigm shift in developing new therapeutic modalities moving towards a more personalized and targeted approach. The tumor-agnostic philosophy, one of these new modalities, focuses on characteristic molecular signatures of transformed cells independently of their traditional histopathological classification. These include commonly occurring DNA aberrations in cancer cells, shared metabolic features of their homeostasis or immune evasion measures of the tumor tissues. The first dedicated, FDA-approved tumor-agnostic agent’s profound progression-free survival of 78% in mismatch repair-deficient colorectal cancer paved the way for the accelerated FDA approvals of novel tumor-agnostic therapeutic compounds. Here, we review the historical background, current status, and future perspectives of this new era of clinical oncology. Full article
(This article belongs to the Special Issue Novel Therapeutic Targets and Approaches, Genetic Markers and Signaling Pathways in Neoplasms)
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25 pages, 3282 KiB  
Review
Molecular Regulation and Oncogenic Functions of TSPAN8
by Jicheng Yang, Ziyan Zhang, Joanne Shi Woon Lam, Hao Fan and Nai Yang Fu
Cells 2024, 13(2), 193; https://doi.org/10.3390/cells13020193 - 19 Jan 2024
Cited by 1 | Viewed by 3706
Abstract
Tetraspanins, a superfamily of small integral membrane proteins, are characterized by four transmembrane domains and conserved protein motifs that are configured into a unique molecular topology and structure in the plasma membrane. They act as key organizers of the plasma membrane, orchestrating the [...] Read more.
Tetraspanins, a superfamily of small integral membrane proteins, are characterized by four transmembrane domains and conserved protein motifs that are configured into a unique molecular topology and structure in the plasma membrane. They act as key organizers of the plasma membrane, orchestrating the formation of specialized microdomains called “tetraspanin-enriched microdomains (TEMs)” or “tetraspanin nanodomains” that are essential for mediating diverse biological processes. TSPAN8 is one of the earliest identified tetraspanin members. It is known to interact with a wide range of molecular partners in different cellular contexts and regulate diverse molecular and cellular events at the plasma membrane, including cell adhesion, migration, invasion, signal transduction, and exosome biogenesis. The functions of cell-surface TSPAN8 are governed by ER targeting, modifications at the Golgi apparatus and dynamic trafficking. Intriguingly, limited evidence shows that TSPAN8 can translocate to the nucleus to act as a transcriptional regulator. The transcription of TSPAN8 is tightly regulated and restricted to defined cell lineages, where it can serve as a molecular marker of stem/progenitor cells in certain normal tissues as well as tumors. Importantly, the oncogenic roles of TSPAN8 in tumor development and cancer metastasis have gained prominence in recent decades. Here, we comprehensively review the current knowledge on the molecular characteristics and regulatory mechanisms defining TSPAN8 functions, and discuss the potential and significance of TSPAN8 as a biomarker and therapeutic target across various epithelial cancers. Full article
(This article belongs to the Special Issue Novel Therapeutic Targets and Approaches, Genetic Markers and Signaling Pathways in Neoplasms)
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