CD68+HLA-DR+ M1-like macrophages promote motility of HCC cells via NF-κB/FAK pathway

Wang, Hao; Wang, Xianteng; Li, Xia; Yong-sheng, Fan; Li, Guosheng; Guo, Chun; Zhu, Faliang; Zhang, Lining; Shi, Yongyu

doi:10.1016/j.canlet.2013.11.013

Cited by 80 publications

(73 citation statements)

References 38 publications

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“…TAMs can promote progression and metastasis through the release of a variety of chemokines, inflammatory factors, and growth factors. It is reported that CD68 + HLA-DR + TAMs in hepatocellular carcinoma (HCC) can promote migration of HCC cells via the NF- κ B/FAK pathway [66]. Specifically, TAM-derived IL-6 and IL-8 enhance invasive activity of LoVo cells induced by PRL-3 in a KCNN4 channel-dependent manner [67].…”

Section: Tams Remodel the Tumor Microenvironmentmentioning

confidence: 99%

New Mechanisms of Tumor-Associated Macrophages on Promoting Tumor Progression: Recent Research Advances and Potential Targets for Tumor Immunotherapy

Guo

Zhichao

Yuan

et al. 2016

Journal of Immunology Research

116

107

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The majority of basic and clinical studies have shown a protumor function of tumor-associated macrophages (TAMs), which represent a large proportion of matrix cells. TAMs promote tumorigenesis, and their number is related to the malignancy degree and poor prognosis of many kinds of tumors. Macrophage plasticity makes it possible to change the tumor microenvironment and remodel antitumor immunity during cancer immunotherapy. Increasing numbers of studies have revealed the effects of TAMs on the tumor microenvironment, for example, via promotion of tumor growth and tumorigenesis and through an increase in the number of cancer stem cells or via facilitation of angiogenesis, lymphangiogenesis, and metastasis. Investigators also proposed tumor-immunological treatments targeting TAMs by inhibiting TAM recruitment and differentiation, by regulating TAM polarization, and by blocking factors and pathways associated with the protumor function of TAMs. This comprehensive review presents recent research on TAMs in relation to prediction of poor outcomes, remodeling of the tumor immune microenvironment, and immunological targeted therapies.

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Section: Tams Remodel the Tumor Microenvironmentmentioning

confidence: 99%

New Mechanisms of Tumor-Associated Macrophages on Promoting Tumor Progression: Recent Research Advances and Potential Targets for Tumor Immunotherapy

Guo

Zhichao

Yuan

et al. 2016

Journal of Immunology Research

116

107

View full text Add to dashboard Cite

show abstract

“…There are, however, a number of aberrant biological mechanisms that contribute to the onset, growth, progression, and metastasis of HCC (Burkhart et al, ; Galuppo et al, ; Jiang et al, ; Yu et al, ). One of the most prominently dysregulated pathways in HCC is the NF‐κB pathway, which likely contributes greatly to the morbidity and mortality of the disease (Li, Tan, Zenali, & Brown, ; Wang et al, , ). Understanding how this pathway is regulated in the development of HCC is therefore crucial to progressing toward improved HCC treatment.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA CASC2 regulates hepatocellular carcinoma cell oncogenesis through miR‐362‐5p/Nf‐κB axis

Zhao

Zhang

2018

Journal Cellular Physiology

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The long non-coding RNA segment cancer susceptibility candidate 2 (CASC2) has been shown to suppress tumor growth in a variety of cancers, including hepatocellular carcinoma (HCC). However, the mechanism by which CASC2 exerts control over HCC has yet to be established. In the present study, we first demonstrated that CASC2 is downregulated in human HCC tissues and HCC cell lines as compared to adjacent non-tumor tissues (NTTs) and a liver cell line, respectively. After finding that CASC2 knockdown significantly promotes HCC cells migration and invasion as well as that CASC2 overexpression inhibits cell migration and invasion, we identified the microRNA miR-362-5p as an endogenous target of CASC2. Through the use of wild type and mutant CASC2 binding sites inserted into psiCHECK-2 luciferase reporter plasmids, as well as qRT-PCR, we determined that CASC2 overexpression reduces miR-362-5p expression levels, while inhibiting CASC2 activity increases miR-362-5p expression. Past research has shown that miR-362-5p stimulates the NF-κB pathway, which has been implicated in the survival and proliferation of a variety of cancer cells. We therefore investigated the effects of CASC2 expression on NF-κB pathway activity. Ultimately, we determined that CASC2 regulates HCC cell activity by targeting miR-362-5p and thus inhibiting the NF-κB pathway. The present study not only identifies CASC2 as an important HCC cell regulator, but also suggests its mechanism of action. It therefore provides the basis for designing strategies to target CASC2 activity and thereby inhibit HCC growth and progression.

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“…Concurrently, high level of NF-κB signaling and activity promote migration and invasive abilities of liver cancer cells (50). Moreover, NF-κB pathway is involved on reduced radiotherapeutics and chemotherapeutics sensitivity of HCC cells (51).…”

Section: P65mentioning

confidence: 99%

SUMOylation and phosphorylation cross-talk in hepatocellular carcinoma

Tomasi

Ramani

2018

Transl. Gastroenterol. Hepatol.

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CD68+HLA-DR+ M1-like macrophages promote motility of HCC cells via NF-κB/FAK pathway

Cited by 80 publications

References 38 publications

New Mechanisms of Tumor-Associated Macrophages on Promoting Tumor Progression: Recent Research Advances and Potential Targets for Tumor Immunotherapy

New Mechanisms of Tumor-Associated Macrophages on Promoting Tumor Progression: Recent Research Advances and Potential Targets for Tumor Immunotherapy

Long noncoding RNA CASC2 regulates hepatocellular carcinoma cell oncogenesis through miR‐362‐5p/Nf‐κB axis

SUMOylation and phosphorylation cross-talk in hepatocellular carcinoma

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