lncRNA-Xist/miR-101-3p/KLF6/C/EBPα axis promotes TAM polarization to regulate cancer cell proliferation and migration

Zhao, Yimeng; Yu, Zhaojin; Ma, Rong; Zhang, Yifan; Zhao, Lin; Yan, Yuanyuan; Lv, Xuemei; Zhang, Liwen; Su, Panpan; Bi, Jia; Xu, Hong; He, Miao; Wei, Minjie

doi:10.1016/j.omtn.2020.12.005

Cited by 95 publications

(58 citation statements)

References 48 publications

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“…These include KLF6, Zeb1 and NFAT1. KLF6 is a transcriptional regulator of macrophage polarization that serves as a phenotypic switch to transform M2-polarized TAMs to M1, effectively inhibiting tumor proliferation and migration (192). Contrariwise, ZEB1 is associated with TAM pro-tumoral activity, indicated by its ability to pioneer epithelial to mesenchymal transition to maintain tumor progression and initiate metastasis (8).…”

Section: Macrophage Polarization By Targeting Intracellular Signaling Mechanismsmentioning

confidence: 99%

Mechanisms of Macrophage Plasticity in the Tumor Environment: Manipulating Activation State to Improve Outcomes

et al. 2021

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Macrophages are a specialized class of innate immune cells with multifaceted roles in modulation of the inflammatory response, homeostasis, and wound healing. While developmentally derived or originating from circulating monocytes, naïve macrophages can adopt a spectrum of context-dependent activation states ranging from pro-inflammatory (classically activated, M1) to pro-wound healing (alternatively activated, M2). Tumors are known to exploit macrophage polarization states to foster a tumor-permissive milieu, particularly by skewing macrophages toward a pro-tumor (M2) phenotype. These pro-tumoral macrophages can support cancer progression by several mechanisms including immune suppression, growth factor production, promotion of angiogenesis and tissue remodeling. By preventing the adoption of this pro-tumor phenotype or reprogramming these macrophages to a more pro-inflammatory state, it may be possible to inhibit tumor growth. Here, we describe types of tumor-derived signaling that facilitate macrophage reprogramming, including paracrine signaling and activation of innate immune checkpoints. We also describe intervention strategies targeting macrophage plasticity to limit disease progression and address their implications in cancer chemo- and immunotherapy.

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Section: Macrophage Polarization By Targeting Intracellular Signaling Mechanismsmentioning

confidence: 99%

Mechanisms of Macrophage Plasticity in the Tumor Environment: Manipulating Activation State to Improve Outcomes

et al. 2021

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“…Ectopic expression of miR-7 was shown to bind directly to XIST and reduce its expression and to reduce BC stem cell-driven tumor growth in vivo [ 231 ]. Consistently with its tumor suppressor role, the knockdown of XIST increased M1-to-M2 macrophage phenotype polarization and promoted the cell proliferation and migration of breast and ovarian cancer cells by competing with miR-101 and inhibiting C/EBPα and KLF6 expression [ 232 ].…”

Section: Resultsmentioning

confidence: 99%

Identification and Roles of miR-29b-1-3p and miR29a-3p-Regulated and Non-Regulated lncRNAs in Endocrine-Sensitive and Resistant Breast Cancer Cells

Muluhngwi

Klinge

2021

Cancers

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Despite improvements in the treatment of endocrine-resistant metastatic disease using combination therapies in patients with estrogen receptor α (ERα) primary tumors, the mechanisms underlying endocrine resistance remain to be elucidated. Non-coding RNAs (ncRNAs), including microRNAs (miRNA) and long non-coding RNAs (lncRNA), are targets and regulators of cell signaling pathways and their exosomal transport may contribute to metastasis. Previous studies have shown that a low expression of miR-29a-3p and miR-29b-3p is associated with lower overall breast cancer survival before 150 mos. Transient, modest overexpression of miR-29b1-3p or miR-29a-3p inhibited MCF-7 tamoxifen-sensitive and LCC9 tamoxifen-resistant cell proliferation. Here, we identify miR-29b-1/a-regulated and non-regulated differentially expressed lncRNAs in MCF-7 and LCC9 cells using next-generation RNA seq. More lncRNAs were miR-29b-1/a-regulated in LCC9 cells than in MCF-7 cells, including DANCR, GAS5, DSCAM-AS1, SNHG5, and CRND. We examined the roles of miR-29-regulated and differentially expressed lncRNAs in endocrine-resistant breast cancer, including putative and proven targets and expression patterns in survival analysis using the KM Plotter and TCGA databases. This study provides new insights into lncRNAs in endocrine-resistant breast cancer.

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“…LncRNAs can function as oncogenes or tumor suppressor genes, and thus are involved in the occurrence and development of many different tumor types. Several lncRNAs are potential diagnostic and/or prognostic biomarkers including lncRNA HOTAIR 174 , lncRNA MALAT1 175 , lncRNA MEG3 176 , lncRNA PVT1 177 , lncRNA XIST 178 , and H19 27 . Although H19 is one of the most studied lncRNAs, many molecular mechanisms remain unelucidated.…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

LncRNA H19: A novel oncogene in multiple cancers

Yang¹,

Qi²,

Fei³

et al. 2021

Int. J. Biol. Sci.

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Long non-coding RNAs (lncRNAs) are a series of non-coding RNAs that lack open reading frameworks. Accumulating evidence suggests important roles for lncRNAs in various diseases, including cancers. Recently, lncRNA H19 (H19) became a research focus due to its ectopic expression in human malignant tumors, where it functioned as an oncogene. Subsequently, H19 was confirmed to be involved in tumorigenesis and malignant progression in many tumors and had been implicated in promoting cell growth, invasion, migration, epithelial-mesenchymal transition, metastasis, and apoptosis. H19 also sequesters some microRNAs, facilitating a multilayer molecular regulatory mechanism. In this review, we summarize the abnormal overexpression of H19 in human cancers, which suggests wide prospects for further research into the diagnosis and treatment of cancers.

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lncRNA-Xist/miR-101-3p/KLF6/C/EBPα axis promotes TAM polarization to regulate cancer cell proliferation and migration

Cited by 95 publications

References 48 publications

Mechanisms of Macrophage Plasticity in the Tumor Environment: Manipulating Activation State to Improve Outcomes

Mechanisms of Macrophage Plasticity in the Tumor Environment: Manipulating Activation State to Improve Outcomes

Identification and Roles of miR-29b-1-3p and miR29a-3p-Regulated and Non-Regulated lncRNAs in Endocrine-Sensitive and Resistant Breast Cancer Cells

LncRNA H19: A novel oncogene in multiple cancers

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