The pathological role of C-X-C chemokine receptor type 4 (CXCR4) in colorectal cancer (CRC) progression; special focus on molecular mechanisms and possible therapeutics

Hjazi, Ahmed; Nasir, Faryal; Noor, Rabia; Alsalamy, Ali; Zabibah, Rahman S.; Romero-Parra, Rosario Mireya; Ullah, Muhammad Ikram; Mustafa, Yasser Fakri; Qasim, Maytham T.; Akram, Shaik Vaseem

doi:10.1016/j.prp.2023.154616

Cited by 9 publications

(1 citation statement)

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“…A study in CRC discovered that, combined blockade of VEGFR and COX2 augmented antiangiogenic, antitumoral and anti-CSC effects, indicating VEGF’s role in maintaining CSC properties ( Zhao et al, 2015a ). Other pro-angiogenic substances secreted by CAFs include platelet-derived growth factor (PDGF), CXCL12, fibroblast growth factor 2 (FGF2), HGF and TGFβ ( Anderberg et al, 2009 ; Wang et al, 2019a ; Kobayashi et al, 2019 ; Hjazi et al, 2023 ).…”

Section: Tumor Microenvironmentmentioning

confidence: 99%

Tumor cell stemness in gastrointestinal cancer: regulation and targeted therapy

Yang,

2024

Front. Mol. Biosci.

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The cancer stem cells are a rare group of self-renewable cancer cells capable of the initiation, progression, metastasis and recurrence of tumors, and also a key contributor to the therapeutic resistance. Thus, understanding the molecular mechanism of tumor stemness regulation, especially in the gastrointestinal (GI) cancers, is of great importance for targeting CSC and designing novel therapeutic strategies. This review aims to elucidate current advancements in the understanding of CSC regulation, including CSC biomarkers, signaling pathways, and non-coding RNAs. We will also provide a comprehensive view on how the tumor microenvironment (TME) display an overall tumor-promoting effect, including the recruitment and impact of cancer-associated fibroblasts (CAFs), the establishment of an immunosuppressive milieu, and the induction of angiogenesis and hypoxia. Lastly, this review consolidates mainstream novel therapeutic interventions targeting CSC stemness regulation.

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