Biological implications of decoding the extracellular matrix of vulva cancer
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- Published online on: December 6, 2024 https://doi.org/10.3892/or.2024.8852
- Article Number: 19
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Copyright: © Islam et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
Abstract
Introduction
Vulvar cancer is the fourth most prevalent gynecological cancer globally, representing 5% of lower genital tract tumors and ranking below uterine corpus, ovarian and cervical cancer (1–3). Key contributors to vulvar cancer development include age, human papillomavirus (HPV) infection, smoking, inflammatory vulvar conditions, prior pelvic radiation, immunodeficiency and anogenital warts (4–6). Among the different histological types of vulvar cancer, vulvar squamous cell carcinoma (VSCC) is the most common type (95%), followed by melanoma, sarcoma and basal cell carcinoma (2,3). VSCC has traditionally been regarded as a disease of postmenopausal women, although the mean age of incidence has fallen in recent years worldwide owing to the increase in HPV infections (1). Nonetheless, the age-specific incidence ranges from 0.4 per 100,000 in younger women to 20 per 100,000 in women >70 years old (7).
VSCC manifests in two types with different pathways: The basaloid and/or warty type often associated with HPV (HPV subtypes 16, 18, 31 and 33) which is predisposed from usual vulvar intraepithelial neoplasia (uVIN), and the second type linked to chronic vulvar dermatoses and differentiated vulvar intraepithelial neoplasia (dVIN) (8). Common TP53 mutations are observed in the second type and are mostly independent of HPV (8). Although there are survival differences in these two types of VSCC, treatment is predominantly surgery with or without radio-chemotherapy. Immunotherapy has reformed the therapeutic paradigms of multiple malignancies, but its impact is limited in VSCC (1). In addition, treatment of unresectable/metastatic disease often leads to frequent comorbidities, particularly in elderly and frail women, highlighting the need for innovative and more effective treatment approaches.
Carcinomas comprise both malignant and non-malignant cells, including fibroblasts, immune cells, vascular cells and neuronal cells (9). Non-malignant cells actively shape the tumor microenvironment (TME) by secreting cytokines, chemokines, growth factors and extracellular matrix (ECM) proteins (9). Under normal physiological conditions, resident cells maintain tissue balance through ECM deposition, degradation and remodeling (10). However, carcinogenesis disrupts ECM remodeling, creating a dysfunctional ECM conducive to a supportive TME that promotes cancer growth, invasion and metastasis (11). While specific research on ECM proteins in VSCC is limited, studies are starting to explore the role of ECM remodeling in VSCC invasion and metastasis.
The present review aims to provide an overview on the role of ECM during VSCC metastasis and the current understanding of the role of ECM in regulating VSCC dissemination. The present study also explored the therapeutic potential of targeting ECM in other types of squamous-epithelial cancers, and the potential prognostic and predictive biomarkers, discussing their impact on developing more efficacious antitumor therapies.
Overview of ECM components
The ECM is commonly defined as the non-malignant, non-cellular component of tissue that provides essential biochemical and structural support to its cellular constituents (12,13). Emerging research suggests that the ECM is not merely an intercellular filler but a physiologically active component of living tissue, playing crucial roles in cell-cell communication, adhesion and proliferation (14,15). Resident fibroblasts are responsible for creating and arranging ECM components according to the specific needs of the tissue (14,16). Major components of the ECM, including collagen, laminin, elastin and proteoglycans, exhibit distinct physical and biochemical properties. A detailed overview of ECM components is shown in Table I.
ECM remodeling in tumorigenesis
Dysregulation of the ECM is a critical factor in cancer development and progression, influencing various key mechanisms. One such mechanism is cellular signaling, where abnormalities in the ECM contribute to uncontrolled cell growth, survival and proliferation, all fundamental cancer hallmarks (14). Moreover, the ECM plays a critical role in cell adhesion and migration, facilitated by proteins such as integrins and cadherins. Disruption of these processes promotes the invasion of cancer cells into surrounding tissues (Fig. 1A) (10). The ECM also affects the immune response within TME, contributing to immune evasion by cancer cells (14). It has been shown that ECM components impede and educate immune cell types such as natural killer cells, macrophages and tumor-infiltrating lymphocytes, specifically CD8+ T cells, within the TME and evade the antitumor immune response (14,17,18). Components such as cross-linked collagen, fibronectin, laminin, periostin, osteopontin, integrins and matrix metalloproteinases (MMPs) can erect physical barriers, hindering immune cell movement and impairing the ability of immune cells such as cytotoxic CD8+ T-cells to target and eliminate cancer cells (Fig. 1B) (19,20).
Understanding the intricate interplay between tumorigenesis and the ECM is essential for developing targeted therapeutic approaches. Fig. 1C illustrates the significant involvement of ECM components in various cancer hallmarks. Over time, intensive research has been dedicated to exploring interventions targeting ECM components or disrupting ECM-associated signaling pathways in tumors originating from squamous epithelia. These endeavors have yielded valuable scientific insights, which are outlined in Table II, and offer promising directions for advancing SCCs treatment (21–102).
Navigating the matrix: Understanding ECM dynamics in vulvar cancer
The ECM in VSCC is a dynamic and influential factor in tumor development (11). This intricate network of proteins, including collagens, laminin, osteopontin, dystroglycan, integrin, CD44 and MMPs, significantly contributes to the progression of VSCC (11). Fig. 1D provides a concise summary of the roles of specific ECM proteins in VSCC and their effects on the hallmarks of cancer. These hallmarks include invasion and metastasis, resistance to cell death, promotion of inflammation, facilitation of replicative immortality and evasion of immune destruction. Thus, understanding the ECM landscape in VSCC can provide valuable insights into the molecular mechanisms underlying this type of cancer.
In order to decipher key ECM proteins involved in VSCC progression, a thorough literature search was performed in the present study. The following MeSH terms were used in PubMed (https://pubmed.ncbi.nlm.nih.gov/), Scopus (https://www.scopus.com/home.uri) and Web of Science (https://mjl.clarivate.com/home) to select literature describing ECM and VSCC tumor progression and development: (‘genital neoplasms, female’[MeSH Terms] OR ‘female genital neoplasm*’[All Fields] OR ‘Gynaecologic neoplasm*’[All Fields] OR ‘Vulvar Neoplasms’[MeSH Terms] OR ‘vulvar neoplasm*’[All Fields] OR ‘vulva neoplasm*’[All Fields] OR ‘cancer of vagina*’[All Fields] OR ‘cancer of vulva*’[All Fields] OR ‘vulva squamous cell carcinoma*’[All Fields] OR ‘vaginal neoplasm*’[All Fields] OR ‘vagina cancer*’[All Fields]) AND (‘Extracellular Matrix’[MeSH Terms] OR ‘extracellular matrix*’[All Fields] OR ‘extracellular matrix protein*’[All Fields]) AND 1980/01/01:2023/12/31 [date-publication]. In the following section, each of the ECM proteins implicated in VSCC progression are described in detail. Table III (103–115) summarizes the key findings regarding ECM proteins in VSCC. This table provides a concise overview of the significant associations, functional implications and clinical relevance of ECM proteins identified in VSCC.
Collagens
Collagens, which are the predominant component of the ECM, are widely distributed across various types of tissue. With 28 different types, the collagen superfamily forms fibers, networks and filaments within the ECM, interacting with mesenchymal-origin cells through various receptor families to regulate their proliferation, migration and differentiation (116). While studies have extensively investigated the role of collagens in driving cancer invasion and metastasis, their specific involvement in VSCC remains understudied. Recent research utilizing Second Harmonic Generation imaging has analyzed collagen parameters (quantity, uniformity and organization) in VSCC, revealing associations with lymph node metastasis (103). Additionally, based on collagen organization, two morphologic variants have been identified in VSCC: An indolent type growing as ‘sheets of cells’ with a pushing border in lymphoplasmacytic stroma, and an aggressive variant growing as ‘single tumor cells’ with a finger-like border in fibromyxoid stroma (104). Proteomic analyses have further demonstrated that the aggressive variants are associated with higher rates of lymph node metastasis and tumor recurrences. Consistent with these findings, previous studies have shown a significant correlation between the ‘sheet of cells’ morphology, HPV infection and improved survival rate (8). Collectively, these findings suggest that morphological variants of collagen fibers in the TME may serve as prognostic indicators for aggressive VSCC. This highlights the potential significance of collagen parameters in understanding VSCC aggressiveness and may offer insights into therapeutic strategies targeting the tumor microenvironment.
Laminins
The laminin family, comprising of ~20 glycoproteins, forms a cross-linked web intertwined with the type IV collagen network in basement membranes. Laminins are heterotrimers composed of three polypeptide chains (α, β, γ) and play crucial roles in early embryonic development, organogenesis and various cell type-specific functions such as adhesion, differentiation, migration, phenotype maintenance and resistance to apoptosis (15). However, in tumors of the lower female genital tract, laminin expression becomes dysregulated (117). Prior research has emphasized that elevated expression of the γ2 chain of laminin-5 (LAMC2) is linked to patient survival in VSCC. Notably, intracytoplasmic expression of the γ2 chain along the invasive tumor front correlates with short-term survival. Larger tumors tend to exhibit increased γ2 chain expression, although no significant correlation has been observed with tumor staging. These findings suggest that heightened expression of the γ2 chain may be involved in the initiation of VSCC tumorigenesis rather than progression (115). However, further investigations are warranted to elucidate the dynamics of LAMC2 in VSCC tumorigenesis.
Osteopontin
Matricellular proteins form a diverse family of non-structural matrix glycoproteins, including thrombospondins, secreted acidic protein and rich in cysteine, tenascins, fibulins, osteopontin, cartilage oligomeric matrix protein and CNN family proteins such as periostin and R-spondins (116). Among these, osteopontin (OPN), initially identified as a bone matrix protein, is now recognized as a cytokine produced by activated T cells and transformed cells. It is highly inducible as it is expressed and secreted by both tumor cells and cells in the stroma (105). In VSCC, OPN expression was investigated across various stages of vulvar lesions, including VSCC, VIN, vulvar lichen sclerosus (VLS) and normal vulvar tissue samples. Proteomic analysis revealed a gradual increase in OPN expression from VIN to VLS, with the highest expression observed in VSCC tumor tissue samples. Additionally, OPN expression was found to be associated with the pathological stage, suggesting its potential role in VSCC tumor progression through neoplastic transformation (105). Collectively, this observation suggested that OPN could be a predictive biomarker for the early detection of VSCC, and further studies are required to understand VSCC pathogenesis through OPN.
Dystroglycan
Dystroglycan, a transmembrane glycoprotein, serves as a crucial link between the ECM and the intracellular cytoskeleton, thereby providing structural integrity. Comprising α and β components, dystroglycan facilitates cell adhesion to the ECM and plays a pivotal role in regulating cytoskeletal organization (118,119). Dysregulation of dystroglycan is a common occurrence observed in various human epithelial cancers, suggesting its potential involvement in tumor development (118,119). Notably, previous research has revealed disrupted expression levels of α-dystroglycan in conditions such as VLS, squamous cell hyperplasia, VIN and invasive VSCC. Specifically, decreased expression of α-dystroglycan has been observed across preneoplastic lesions of VSCC, and this downregulation is associated with advanced stages of VSCC. These findings suggest that α-dystroglycan may play a significant role in maintaining cytoskeletal dynamics, and its reduced expression could promote VSCC progression (106).
Integrins β1
Integrins, heterodimeric receptors comprising α and β subunits, are frequently dysregulated in skin cancers (107). Serving as bridging molecules, integrins connect ECMs with the cell cytoskeleton, governing cell adhesion and motility. The intracellular tail of integrin β1 associates with proteins such as talin, α-actinin and vinculin, linking it to the actin cytoskeleton and regulating cell motility, keratinocyte wound healing and the collective movement of tumor cells (115). Increased expression of various integrin (ITG) family proteins, including α2, α3, α5, α6 and β1 has been observed in VSCC. Among these, β1 (ITGB1) plays a pivotal role in mediating cell adhesion, migration and invasion (107). Knockdown experiments targeting β1 result in significant alterations in VSCC tumor morphology compared with control tumors. Specifically, β1 knockdown leads to a more encapsulated and less invasive tumor phenotype, indicating the crucial involvement of integrin β1 in VSCC invasiveness and disease progression (107). The present study underscores the significance of β1 integrin in VSCC tumor advancement and suggests potential therapeutic avenues for intervention.
Hyaluronic acid receptor CD44
Hyaluronic acid receptor CD44 is a surface-expressed glycoprotein that facilitates interactions with a spectrum of molecules, including collagen, fibronectin, OPN, MMPs and growth factors (70,71). CD44 plays a pivotal role in cell adhesion, interactions, migration and metastasis. CD44 isoforms bolster malignant cell affinity to ECM ligands, thereby fostering tumor dissemination (70,71). A previous study has demonstrated a significant association between CD44 variants, particularly CD44v3 and CD44v6 and VSCC tumor progression, as well as adverse patient outcomes (108). Elevated CD44 expression correlates with poor tumor differentiation, positive lymph node involvement, advanced-stage VSCC and diminished survival rates, indicating its potential as a prognostic marker (108).
MMPs
MMPs are a family of calcium-dependent, zinc-containing endopeptidases that target various molecules, including matrix components, growth factors, cytokines and signaling molecules. Synthesized as zymogens, MMPs are secreted after cleavage of their propeptide form. Invasion and metastasis of malignant cells involve the degradation of the stromal matrix, mediated by specific MMPs (120).
MMP2
MMP2 plays a pivotal role in degrading crucial components of basement membranes such as type IV collagen and fibronectin, facilitating the invasion of tumor cells into stromal and vascular regions (25,110). Overexpression of MMP2 has been observed across various disease stages of VSCC, including VIN (grades-I, II, III) and VLS and this heightened expression is significantly associated with the invasiveness of VSCC (110). Morphologically, MMP2 manifests as cytoplasmic granular or diffuse staining in stromal cells. However, in cases of invasive VSCC, MMP2-positive cells are notably observed in the stroma adjacent to neoplastic islands or infiltrating groups of tumor cells (110). These highly MMP2-expressing tumor cells secrete factors that contribute to the aggressiveness of VSCC, including invasion and metastasis, suggesting potential therapeutic approaches targeting MMP2.
MMP12
MMP12, recognized for its ability to degrade elastin and various substrates such as type IV collagen, fibronectin and laminin, plays a multifaceted role in cancer progression, particularly in VSCC. It contributes to limiting tumor growth by converting plasminogen into angiostatin, which inhibits endothelial cell proliferation and angiogenesis, essential processes for tumor vascularization (111). While typically associated with macrophages, MMP12 is also expressed by transformed epithelial cells in VSCC, with its expression level correlating with tumor dedifferentiation and histological aggressiveness (112). In a study involving 33 VSCC samples, MMP12 mRNA was prevalent, and higher expression in cancer cells was associated with more aggressive and poorly differentiated tumors (112). Notably, macrophage-derived MMP12 was more abundant in well-differentiated grade I tumors compared with grade III tumors (112). These findings suggest MMP12 potential role in modulating VSCC histology and influencing treatment strategies. However, further research is warranted to fully understand MMP12 implications in VSCC and its therapeutic relevance.
MMP13
MMP13, recognized for its ability to cleave fibrillar collagens and various stromal matrix components, stands out as a versatile proteolytic tool crucial for tumor cell invasion (16,116,120,121). A previous study has highlighted the abundant expression of MMP13 in VSCC tumor tissues, often correlating with lymph node metastasis (109). Moreover, in vitro investigations have revealed a significant increase in MMP13 levels in VSCC cell lines compared with control epithelial cells (109). These findings underscore MMP13 specific expression by malignantly transformed squamous epithelial cells, including VSCC cells, suggesting its potential as a marker for their invasive potential (109).
Elucidating molecular synergies: Cancer-associated fibroblasts (CAFs) and ECM in VSCC progression
Fibroblasts are the main architects of the ECM, orchestrating changes that play a major role in tumor progression, inflammation, therapy resistance and immunosuppression (9,122). CAFs are perhaps the cells most proficient at remodeling the ECM as they deposit collagens and release various growth factors, chemokines, cytokines and MMPs (Fig. 1A). Significantly altered gene pathways in CAFs include regulation of substrate adhesion, tissue remodeling, cell migration, secretion, growth regulation and angiogenesis (123). Although, at present, VSCC-specific subpopulations of CAFs have not been reported, single-cell RNA sequencing data suggests that various CAF subpopulations exist in the TME of other types of SCCs (124,125).
The most commonly identified CAF subpopulations are those involved in ECM remodeling [myofibroblast CAFs (myCAFs)] and immunomodulatory cancer-associated fibroblasts] (126). MyCAFs have been reported to be involved in tissue remodeling and often express ACTA2 gene (126). Inflammatory CAFs often exhibit increased IL-6 signaling in various tumor types (126–129). This makes them potential targets for anti-IL-6 therapies, such as siltuximab and tocilizumab (130). Moreover, research has shown that immunoregulatory CAFs can activate JAK-STAT signaling in cancer cells (129), suggesting that inhibition of this pathway may be a promising therapeutic strategy.
Mounting evidence suggests that CAFs also play a key role in therapy-resistance in SCCs, particularly in head and neck SCC (HNSCC) and esophageal SCC (131–133). It has been previously reported that chemotherapy promotes CAF survival and alters exosome biogenesis, which leads to malignant characteristics in HNSCC (134). Notably, CAFs also respond to radiotherapy by upregulating transforming growth factor β1 (TGFβ1) expression via IL-8/NF-κB signaling in HNSCC, which increases the rate of invasive growth. This signaling can be inhibited by using Tranilast, a known TGFβ1 inhibitor (135). A subset of CAFs have also been reported to be involved in TGFβ1 dependent PD-1+/TIM-3+ exhaustion of CD8 T cells in HNSCC, leading to exclusion of T cells, thereby negatively impacting immunotherapy response (124,136). Previously, we have shown that CAFs play a decisive role in VSCC invasion and that VSCC cells exhibit a fibroblast-dependent tumorigenic potential (137). However, there exists a significant heterogeneity with CAFs showing both tumor-promoting and tumor-inhibiting CAFs (9,122). Gaining a more profound insight into the molecular and phenotypic variations among CAF populations in VSCC may contribute to overcoming challenges related to therapy resistance and the targeting of cancer cells.
Decoding therapeutic prospects: ECM proteins in VSCC
The therapeutic potential of ECM proteins in treating VSCC holds promise for pioneering treatment strategies. Identifying specific ECM proteins involved in VSCC tumorigenesis will unveil potential therapeutic targets. While the pathways linked with ECM proteins in VSCC are not fully understood, emerging bioinformatic platforms (138) provide opportunities to pinpoint key pathways and potential targeted therapies for this relatively underexplored cancer. Notably, these proteins, irrespective of ECM organization, are implicated in modulating immune systems, as depicted in Fig. 2.
Despite the absence of reports on ECM proteins regulating immune compartments in VSCC, insights from other epithelial-origin tumors in The Cancer Genome Atlas suggests that investigating ECM in VSCC may be beneficial. Bioinformatics platforms such as TIMER2 (http://timer.cistrome.org/) (139) confirm that higher expression levels of ECM-related genes are associated with reduced CD8+ T cell infiltration within the TME, fostering immune evasion and tumor progression across various epithelial cancers (140–143) (Figs. 3 and 4). Consequently, over the last few decades, several ECM inhibitors have been developed and successfully employed across different SCCs (Table IV) (144–158). Therefore, understanding the intricate relationship between ECM components in the context of VSCC is essential for devising innovative therapeutic strategies tailored to this patient population. Such endeavors hold the potential to pave the way for the emergence of novel therapeutics.
Exploring future avenues: Research directions in VSCC and ECM interactions
The present study thoroughly investigated the intricate landscape of the ECM in VSCC, examining the roles of various components such as collagens, laminin, osteopontin, dystroglycan, integrin, CD44 and MMPs in VSCC progression. Furthermore, the present study highlights the evolving understanding of ECM, going beyond its structural role to actively influence adhesion, proliferation and cell communication. Attention is provided to collagen types, emphasizing their structural significance and their correlation with changes in collagen levels and lymph node metastasis in VSCC.
Conclusion
The present study acknowledges the rising incidence of vulvar cancer and the limitations of current treatment approaches, particularly in incurable or metastatic cases. It advocates for the exploration of novel therapeutic pathways and targets based on the detailed analysis of ECM components in VSCC. Recognizing the complex interactions within the TME underscores the necessity for innovative and targeted therapeutic approaches to enhance outcomes for individuals affected by VSCC. Further research and clinical exploration of these ECM targets could pave the way for more effective therapeutic strategies in the management of VSCC.
Acknowledgements
The results shown here are in part based upon data generated by the TCGA Research Network: https://www.cancer.gov/tcga.
Funding
This work was supported by the Research Council of Norway through its Centers of Excellence funding scheme (grant no. 22325).
Availability of data and materials
Not applicable.
Authors' contributions
EI and KCD conducted the literature review and drafted the manuscript. RM, KO, SI and HND contributed to the writing of the manuscript and made corrections. All authors have read and approved the final manuscript. Data authentication is not applicable.
Ethics approval and consent to participate
Not applicable.
Patient consent for publication
Not applicable.
Competing interests
The authors declare that they have no competing interests.
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