Oral Squamous Cell Carcinoma-Derived ANGPTL3 Induces Cancer Associated Fibroblastic Phenotypes in Surrounding Fibroblasts

Kim, Jue Young; Moon, Sook; Kim, Dokyeong

doi:10.31557/apjcp.2022.23.12.4315

Cited by 4 publications

(3 citation statements)

References 31 publications

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“…In addition, it has been shown that ANGPTL3 is highly expressed in hepatocellular carcinoma, 158 ovarian cancer, 159 and oral squamous cell carcinoma, 149 which may be related to the fact that ANGPTL3 induces cancer-associated fibroblasts differentiation. 158,160…”

Section: Structure and Function Of Angptl3mentioning

confidence: 99%

“…Furthermore, ANGPTL3 expression is elevated in the livers of NAFLD patients, 149,157 and its inhibitors have the potential to mitigate the progression of NAFLD and provide promising therapeutic approaches for NAFLD. In addition, it has been shown that ANGPTL3 is highly expressed in hepatocellular carcinoma, 158 ovarian cancer, 159 and oral squamous cell carcinoma, 149 which may be related to the fact that ANGPTL3 induces cancer‐associated fibroblasts differentiation 158,160 …”

Section: Drug Development Of Targets Based On Gwas Wgs and Wes Discov...mentioning

confidence: 99%

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Drug development advances in human genetics‐based targets

Zhang,

Yu,

et al. 2024

MedComm

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Drug development is a long and costly process, with a high degree of uncertainty from the identification of a drug target to its market launch. Targeted drugs supported by human genetic evidence are expected to enter phase II/III clinical trials or be approved for marketing more quickly, speeding up the drug development process. Currently, genetic data and technologies such as genome‐wide association studies (GWAS), whole‐exome sequencing (WES), and whole‐genome sequencing (WGS) have identified and validated many potential molecular targets associated with diseases. This review describes the structure, molecular biology, and drug development of human genetics‐based validated beneficial loss‐of‐function (LOF) mutation targets (target mutations that reduce disease incidence) over the past decade. The feasibility of eight beneficial LOF mutation targets (PCSK9, ANGPTL3, ASGR1, HSD17B13, KHK, CIDEB, GPR75, and INHBE) as targets for drug discovery is mainly emphasized, and their research prospects and challenges are discussed. In conclusion, we expect that this review will inspire more researchers to use human genetics and genomics to support the discovery of novel therapeutic drugs and the direction of clinical development, which will contribute to the development of new drug discovery and drug repurposing.

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Section: Structure and Function Of Angptl3mentioning

confidence: 99%

Section: Drug Development Of Targets Based On Gwas Wgs and Wes Discov...mentioning

confidence: 99%

Drug development advances in human genetics‐based targets

Zhang,

Yu,

et al. 2024

MedComm

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show abstract

“…Another study observed elevated levels of GRO-α and tumor-promoting interleukins corresponding to the expression of angiopoietin-like protein. This can in turn induce CAF-like phenotypes within the stromal fibroblasts of OSCC cells and increase the levels of CAF markers, a-SMA and FAP, making this a potential quarry for targeted therapies in the future ( 105 ).…”

Section: Extrinsic Factors Governing Oscc Stemnessmentioning

confidence: 99%

Panoramic view of key cross-talks underpinning the oral squamous cell carcinoma stemness - unearthing the future opportunities

Vastrad,

Ritesh,

et al. 2023

Front. Oncol.

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The clinical management of oral cancer is often frequented with challenges that arise from relapse, recurrence, invasion and resistance towards the cornerstone chemo and radiation therapies. The recent conceptual advancement in oncology has substantiated the role of cancer stem cells (CSC) as a predominant player of these intricacies. CSC are a sub-group of tumor population with inherent adroitness to self-renew with high plasticity. During tumor evolution, the structural and functional reprogramming persuades the cancer cells to acquire stem-cell like properties, thus presenting them with higher survival abilities and treatment resistance. An appraisal on key features that govern the stemness is of prime importance to confront the current challenges encountered in oral cancer. The nurturing niche of CSC for maintaining its stemness characteristics is thought to be modulated by complex multi-layered components encompassing neoplastic cells, extracellular matrix, acellular components, circulatory vessels, various cascading signaling molecules and stromal cells. This review focuses on recapitulating both intrinsic and extrinsic mechanisms that impart the stemness. There are contemplating evidences that demonstrate the role of transcription factors (TF) in sustaining the neoplastic stem cell’s pluripotency and plasticity alongside the miRNA in regulation of crucial genes involved in the transformation of normal oral mucosa to malignancy. This review illustrates the interplay between miRNA and various known TF of oral cancer such as c-Myc, SOX, STAT, NANOG and OCT in orchestrating the stemness and resistance features. Further, the cross-talks involved in tumor micro-environment inclusive of cytokines, macrophages, extra cellular matrix, angiogenesis leading pathways and influential factors of hypoxia on tumorigenesis and CSC survival have been elucidated. Finally, external factorial influence of oral microbiome gained due to the dysbiosis is also emphasized. There are growing confirmations of the possible roles of microbiomes in the progression of oral cancer. Given this, an attempt has been made to explore the potential links including EMT and signaling pathways towards resistance and stemness. This review provides a spectrum of understanding on stemness and progression of oral cancers at various regulatory levels along with their current therapeutic knowledge. These mechanisms could be exploited for future research to expand potential treatment strategies.

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