Cancer-associated adipocytes promote the invasion and metastasis in breast cancer through LIF/CXCLs positive feedback loop

Zhou, Chong; He, Xi; Tong, Chang; Li, Honghui; Xie, Caifeng; Wu, Yudong; Wang, Lieliang; Yan, Xiaohua; Luo, Daya; Tang, Yunpeng; Cheng, Zhongman; Xiong, Xiangyang

doi:10.7150/ijbs.65227

Cited by 27 publications

(19 citation statements)

References 39 publications

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“…At the same time, TGF-α does not affect the expression of CXCR2 ligands in non-triple-negative breast cancer cells. CXCL1 expression in breast cancer cells is also increased by secretory factors such as prostaglandin E 2 (PGE 2 ) [ 58 ], interleukin-17 (IL-17) derived from T helper type 17 (Th17) cells [ 59 , 60 ], loss of response to transforming growth factor-β (TGF-β) [ 61 , 62 ], tumor necrosis factor-α (TNF-α) [ 42 ], leukemia inhibitory factor (LIF) [ 63 ], plasminogen activator inhibitor-1 (PAI-1) [ 64 ], and Notch signaling [ 65 ].…”

Section: Breast Cancermentioning

confidence: 99%

Involvement in Tumorigenesis and Clinical Significance of CXCL1 in Reproductive Cancers: Breast Cancer, Cervical Cancer, Endometrial Cancer, Ovarian Cancer and Prostate Cancer

Korbecki

Bosiacki

Barczak

et al. 2023

IJMS

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C-X-C motif chemokine ligand 1 (CXCL1) is a member of the CXC chemokine subfamily and a ligand for CXCR2. Its main function in the immune system is the chemoattraction of neutrophils. However, there is a lack of comprehensive reviews summarizing the significance of CXCL1 in cancer processes. To fill this gap, this work describes the clinical significance and participation of CXCL1 in cancer processes in the most important reproductive cancers: breast cancer, cervical cancer, endometrial cancer, ovarian cancer, and prostate cancer. The focus is on both clinical aspects and the significance of CXCL1 in molecular cancer processes. We describe the association of CXCL1 with clinical features of tumors, including prognosis, ER, PR and HER2 status, and TNM stage. We present the molecular contribution of CXCL1 to chemoresistance and radioresistance in selected tumors and its influence on the proliferation, migration, and invasion of tumor cells. Additionally, we present the impact of CXCL1 on the microenvironment of reproductive cancers, including its effect on angiogenesis, recruitment, and function of cancer-associated cells (macrophages, neutrophils, MDSC, and Treg). The article concludes by summarizing the significance of introducing drugs targeting CXCL1. This paper also discusses the significance of ACKR1/DARC in reproductive cancers.

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Section: Breast Cancermentioning

confidence: 99%

Involvement in Tumorigenesis and Clinical Significance of CXCL1 in Reproductive Cancers: Breast Cancer, Cervical Cancer, Endometrial Cancer, Ovarian Cancer and Prostate Cancer

Korbecki

Bosiacki

Barczak

et al. 2023

IJMS

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“…In this respect, breast cancer adipocytes may stimulate the onset of epithelialmesenchymal transition (EMT) in breast cancer cells by expressing exosomal TSP5 [120] [114]. Mechanistically, breast adipocytes protect early breast tumor cells from ferroptosis and other ROS-mediated forms of cell death by secretion of fatty acids [121], and the crosstalk between adipocytes and malignant cells may occur via secretion of leukemia inhibitory factor (LIF) and C-X-C subfamily chemokines in a positive feedback mode [122]. Also, these cancer-associated adipocytes undergo "browning" -the process of increasing the number of mitochondria [123].…”

Section: Hypothesis: Role Of Breast Adipocytes In Early Progression O...mentioning

confidence: 99%

BRCA Mutations: The Achilles Heel of Breast, Ovarian and Other Epithelial Cancers

Loboda¹,

Adonin²,

Zvereva³

et al. 2023

Preprint

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Two related tumor suppressor genes, Brca1 and Brca2, attract a lot of attention from both fundamental and clinical points of view. Oncogenic hereditary mutations in these genes are firmly linked to the early onset of breast and ovarian cancers. However, the molecular mechanisms that drive extensive mutagenesis in these genes are not known. In this review we hypothesize that one of the potential mechanisms behind this phenomenon can be mediated by Alu mobile genomic elements. Linking mutations in the BRCA1 and BRCA2 genes to the general mechanism(s) of genome stability and DNA repair is critical to ensure the rationalized choice of anti-cancer therapy. Accordingly, we review the literature available on mechanisms of DNA damage repair where these proteins are involved in and how the inactivating mutations in these genes (BRCAness) can be exploited in anti-cancer therapy. We also propose a hypothesis that explains why breast and ovarian epithelial tissues are preferentially susceptible to mutations in BRCA genes. Finally, we discuss perspectives of novel therapeutic approaches for treating BRCAness cancers.

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“…In the ovarian cancer microenvironment, cancer-associated mesenchymal stem cells activate the JAK/STAT pathway in ovarian cancer cells by secreting LIF, promoting cancer cell growth, and maintaining their stem cell properties [ 63 ]. In addition, our previous research has verified that LIF is highly expressed in cancer-associated adipocytes (CAA) and forms a feedback loop with the CXCLs derived from breast cancer to promote the invasion and metastasis of breast cancer [ 64 ].…”

Section: Lif and Cancer-associated Cachexiamentioning

confidence: 99%

The Molecular Basis and Therapeutic Potential of Leukemia Inhibitory Factor in Cancer Cachexia

Zeng

Tong

Xiong

2022

Cancers

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Cachexia is a chronic metabolic syndrome that is characterized by sustained weight and muscle mass loss and anorexia. Cachexia can be secondary to a variety of diseases and affects the prognosis of patients significantly. The increase in inflammatory cytokines in plasma is deeply related to the occurrence of cachexia. As a member of the IL-6 cytokine family, leukemia inhibitory factor (LIF) exerts multiple biological functions. LIF is over-expressed in the cancer cells and stromal cells of various tumors, promoting the malignant development of tumors via the autocrine and paracrine systems. Intriguingly, increasing studies have confirmed that LIF contributes to the progression of cachexia, especially in patients with metastatic tumors. This review combines all of the evidence to summarize the mechanism of LIF-induced cachexia from the following four aspects: (i) LIF and cancer-associated cachexia, (ii) LIF and alterations of adipose tissue in cachexia, (iii) LIF and anorexia nervosa in cachexia, and (iv) LIF and muscle atrophy in cachexia. Considering the complex mechanisms in cachexia, we also focus on the interactions between LIF and other key cytokines in cachexia and existing therapeutics targeting LIF.

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Cancer-associated adipocytes promote the invasion and metastasis in breast cancer through LIF/CXCLs positive feedback loop

Cited by 27 publications

References 39 publications

Involvement in Tumorigenesis and Clinical Significance of CXCL1 in Reproductive Cancers: Breast Cancer, Cervical Cancer, Endometrial Cancer, Ovarian Cancer and Prostate Cancer

Involvement in Tumorigenesis and Clinical Significance of CXCL1 in Reproductive Cancers: Breast Cancer, Cervical Cancer, Endometrial Cancer, Ovarian Cancer and Prostate Cancer

BRCA Mutations: The Achilles Heel of Breast, Ovarian and Other Epithelial Cancers

The Molecular Basis and Therapeutic Potential of Leukemia Inhibitory Factor in Cancer Cachexia

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