Upregulation of CELSR1 expression promotes ovarian cancer cell proliferation, migration, and invasion

Zuo, Jiwei; Zheng, Anqi; Wang, Xingyue; Luo, Zhicheng; Chen, Yueming; Cheng, Xiaoxiao; Zhao, Yuemei; Zhou, Xian; Tang, Kai-Fu; Du, Xing

doi:10.1007/s12032-023-02232-1

Cited by 6 publications

(1 citation statement)

References 42 publications

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“…Evidence is accumulating that a human ortholog of Fmi, CELSR3, is expressed at high levels in a range of solid tumors, including lung, prostate, pancreatic, hepatic, ovarian and colorectal cancers, and in some cases has been shown to be associated with poor prognosis (Katoh & Katoh, 2007; Erkan et al, 2010; Asad et al, 2014; Goryca et al, 2018; Li et al, 2021; Chen et al, 2021a). Recently, CELSR1 upregulation has also been linked to poor ovarian cancer prognosis, likely by promoting proliferation, migration, and invasion (Zuo et al, 2023). If CELSR1/3 are promoting winner cell behavior in these tumors, as might be predicted from its function in Drosophila , this could provide the rationale for future efforts to understand the mechanism by which Fmi/CELSR3 facilitates cell competition, with the goal of identifying an intervention that could blunt or perhaps even eliminate the aggressiveness of an array of highly morbid cancers.…”

Section: Discussionmentioning

confidence: 99%

Flamingo participates in multiple models of cell competition

Bosch,

Cho,

Axelrod

2023

Preprint

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The growth and survival of cells with different fitness, such as those with a proliferative advantage or a deleterious mutation, is controlled through cell competition. During development, cell competition enables healthy cells to eliminate less fit cells that could jeopardize tissue integrity, and facilitates the elimination of pre-malignant cells by healthy cells as a surveillance mechanism to prevent oncogenesis. Malignant cells also benefit from cell competition to promote their expansion. Despite its ubiquitous presence, the mechanisms governing cell competition, particularly those common to developmental competition and tumorigenesis, are poorly understood. Here, we show that in Drosophila, the planar cell polarity (PCP) protein Flamingo (Fmi) is required by winners to maintain their status during cell competition in malignant tumors to overtake healthy tissue, in pre-malignant cells as they grow among wildtype cells, in healthy cells to eliminate pre-malignant cells, and by supercompetitors to occupy excessive territory within wildtype tissues. "Would-be" winners that lack Fmi are unable to over-proliferate, and instead become losers. We demonstrate that the role of Fmi in cell competition is independent of PCP, and that it uses a distinct mechanism that may more closely resemble one used in other less well defined functions of Fmi.

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Section: Discussionmentioning

confidence: 99%

Flamingo participates in multiple models of cell competition

Bosch,

Cho,

Axelrod

2023

Preprint

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Pitfalls in identifying intronic germline pathogenic variants by comprehensive cancer genomic profiling: technical limitations or biased clinical/diagnostic utility?

De Bonis,

Nero,

Scambia

et al. 2024

Int J Gynecol Cancer

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Flamingo participates in multiple models of cell competition

Bosch,

Cho,

Axelrod

2024

Preprint

View full text Add to dashboard Cite

The growth and survival of cells with different fitness, such as those with a proliferative advantage or a deleterious mutation, is controlled through cell competition. During development, cell competition enables healthy cells to eliminate less fit cells that could jeopardize tissue integrity, and facilitates the elimination of pre-malignant cells by healthy cells as a surveillance mechanism to prevent oncogenesis. Malignant cells also benefit from cell competition to promote their expansion. Despite its ubiquitous presence, the mechanisms governing cell competition, particularly those common to developmental competition and tumorigenesis, are poorly understood. Here, we show that in Drosophila , the planar cell polarity (PCP) protein Flamingo (Fmi) is required by winners to maintain their status during cell competition in malignant tumors to overtake healthy tissue, in early pre-malignant cells when they overproliferate among wildtype cells, in healthy cells when they later eliminate pre-malignant cells, and by supercompetitors as they compete to occupy excessive territory within wildtype tissues. “Would-be” winners that lack Fmi are unable to over-proliferate, and instead become losers. We demonstrate that the role of Fmi in cell competition is independent of PCP, and that it uses a distinct mechanism that may more closely resemble one used in other less well-defined functions of Fmi.

show abstract

Upregulation of CELSR1 expression promotes ovarian cancer cell proliferation, migration, and invasion

Cited by 6 publications

References 42 publications

Flamingo participates in multiple models of cell competition

Flamingo participates in multiple models of cell competition

Pitfalls in identifying intronic germline pathogenic variants by comprehensive cancer genomic profiling: technical limitations or biased clinical/diagnostic utility?

Flamingo participates in multiple models of cell competition

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