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Inflammation and cancer are intricately linked, with emerging evidence highlighting the complex interplay between these two processes. While inflammation is a natural response aimed at maintaining tissue homeostasis and combating infections, chronic or persistent inflammation has been increasingly associated with the development and progression of various cancers [References]. Within this intricate landscape, a relatively recent focus has emerged on the relationship between inflammation and cancer stem cells (CSCs).

CSCs are a unique subset of cells within a tumor that possess stem cell-like properties, including self-renewal and the ability to give rise to a heterogeneous population of cancer cells. These cells are believed to play a crucial role in tumor initiation, progression, metastasis, and therapy resistance. CSCs share some characteristics with normal stem cells [2], and their presence within tumors adds complexity to our understanding of cancer biology.

Inflammation contributes to cancer development through various mechanisms, including DNA damage, oxidative stress, immune suppression, and promotion of angiogenesis. Tumor-associated inflammation often involves immune cells [3], cytokines, chemokines, and growth factors, collectively creating a microenvironment that supports tumor growth and survival. Recent research has unveiled a connection between inflammation and the maintenance and behavior of CSCs within tumors [4].

Linking inflammation and cancer stem cells

The crosstalk between inflammation and CSCs represents a critical area of investigation in cancer research. Inflammatory signals within the tumor microenvironment can influence CSC properties, including self-renewal, differentiation, and survival. Conversely, CSCs can engage in bidirectional interactions with immune cells and produce inflammatory mediators that contribute to tumor-promoting inflammation [5].

Mechanisms underlying the interaction

Several molecular mechanisms have been proposed to explain the interplay between inflammation and CSCs. Inflammatory cytokines, such as interleukins and tumor necrosis factor-alpha (TNF-α), can activate signaling pathways that sustain CSC self-renewal and survival [6]. Inflammatory mediators may also induce epithelial-mesenchymal transition (EMT), a process associated with increased CSC properties and metastatic potential.

Clinical implications

Understanding the relationship between inflammation and CSCs has significant clinical implications. Targeting inflammation-induced pathways may hold promise as a strategy to disrupt the CSC niche and hinder tumor progression. Moreover, the identification of CSCspecific markers within inflamed tumor microenvironments can aid in the development of targeted therapies aimed at eliminating these resilient cell populations [7].

The intricate interplay between inflammation and cancer stem cells (CSCs) offers intriguing insights into the complex landscape of tumour biology. This section examines the implications of the identified molecular interactions and their potential significance for both basic research and clinical applications.

Molecular crosstalk and signaling pathways

The integration of multiple studies reveals a compelling molecular crosstalk between inflammatory mediators and CSCs. Inflammatory cytokines, such as interleukins and TNF-α, appear to have dual roles, triggering CSC self-renewal and enhancing their survival [8]. This intricate signaling landscape suggests that inflammation contributes to the stemness of CSCs, thus potentially affecting tumor initiation, progression, and metastasis.

Impact on tumour microenvironment

The dynamic interplay between inflammation and CSCs contributes to the formation of a tumor-permissive microenvironment. Inflammatory signals foster the recruitment of immune cells and remodeling of the extracellular matrix, further nurturing CSCs and promoting tumor growth. This symbiotic relationship underscores the importance of understanding the bidirectional communication within the tumor microenvironment [9].

Epithelial-mesenchymal transition (EMT)

Notably, inflammation-induced EMT emerges as a critical mechanism linking inflammation and the acquisition of CSC-like properties. The transition from an epithelial to mesenchymal phenotype enhances CSC characteristics, potentially facilitating metastasis and therapy resistance. Strategies aimed at disrupting this EMT-associated crosstalk may offer new avenues for therapeutic interventions.

Clinical implications and therapeutic strategies

The insights gained from exploring the interplay between inflammation and CSCs hold profound clinical implications. Targeting the inflammation-CSC axis may represent a novel therapeutic approach to inhibit tumor growth and improve treatment outcomes [10]. Developing agents that specifically disrupt inflammatory pathways involved in CSC maintenance could offer a promising strategy to halt disease progression.

Challenges and future directions

While the current body of research provides valuable insights, challenges remain in translating these findings into clinical applications. Understanding the context-dependent effects of inflammation on CSC behavior, deciphering the intricate network of signaling pathways, and identifying specific therapeutic targets present ongoing challenges. Moreover, the potential effects of anti-inflammatory therapies on normal stem cells warrant careful consideration [11 ].

Integration with immunotherapy and precision medicine

Integrating the knowledge gained from inflammation-CSC interactions with emerging immunotherapeutic approaches and precision medicine holds significant promise. Designing strategies that combine immunomodulation with CSC-targeted therapies could enhance the overall efficacy of cancer treatment, potentially improving patient outcomes [12 ].

Conclusion

The intricate relationship between inflammation and cancer stem cells adds a layer of complexity to our understanding of cancer biology and opens new avenues for therapeutic intervention. Investigating the molecular mechanisms underlying this crosstalk could lead to innovative strategies that target both inflammation and CSCs, ultimately improving the efficacy of cancer treatment and patient outcomes. As research in this field continues to evolve, unravelling the dynamic interplay between inflammation and CSCs promises to shed light on novel aspects of cancer progression and provide opportunities for developing personalized and effective therapeutic approaches.

Acknowledgement

None

Conflict of Interest

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1. Ancker JS, Edwards A, Nosal S, Hauser D, Mauer E, et al. (2017) . BMC Medical Informatics and Decision Making 17: 36.

, ,

2. Buchanan AH, Christianson CA, Himmel T, Powell KP, Agbaje A, et al. (2015) . J Genet Couns 24: 179-188.

, ,

3. Caswell-Jin JL, Zimmer AD, Stedden W, Kingham KE, Zhou AY, et al. (2019) . J Natl Cancer Inst 111: 95-98.

, ,

4. Pannala R, Basu A, Petersen GM, Chari ST (2009) . Lancet Oncol 10: 88-95.

, , Crossref

5. Singhi AD, Koay EJ, Chari ST, Maitra A (2019) . Gastroenterology 156: 2024-2040.

, ,

6. Ansary-Moghaddam A, Huxley R, Barzi F (2006) . Cancer Epidemiol Biomarkers Prev 15: 2435-2440.

, ,

7. Vasen H, Ibrahim I, Ponce CG (2016) . J Clin Oncol 34: 2010-2019.

, ,

8. Canto MI, Almario JA, Schulick RD (2018) Risk of neoplastic progression in individuals at high risk for pancreatic cancer undergoing long-term surveillance. Gastroenterology 155: 740-751.

, , Crossref

9. Chhoda A, Vodusek Z, Wattamwar K (2022) . Gastroenterology 162: 786-798.

Indexed at, Google Scholar, Crossref

10. Klatte DCF, Boekestijn B, Wasser M (2022) . J Clin Oncol 40: 3257-3266.

, ,

11. Rosenbaum PR, Rubin DB (1985) . Am Stat 39: 33-38.

, ,

12. Ho D, Imai K, King G (2011) . J Stat Softw 42: 1-28.

, ,