NF-κB pathways are involved in M1 polarization of RAW 264.7 macrophage by polyporus polysaccharide in the tumor microenvironment

Liu, Chunping; Zhang, Xian; Tan, Qinglong; Xú, Wénxìng; Zhou, Chang‐Yuan; Luo, Min; Li, Xiong; Huang, Run‐Yue; Xing, Zhen

doi:10.1371/journal.pone.0188317

Cited by 91 publications

(76 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…M1 macrophage differentiation is involved with the coactivation of the NF‐κB and STAT3 pathways in miR‐15a/16 −/− mice in tumour or inflammation. Polyporus polysaccharide activates the NF‐κB signalling pathway by interfering with IκB phosphorylation for M1 macrophage polarization . P21 regulates macrophage reprogramming by shifting the balance between active p65‐p50 and inhibitory p50‐p50 NF‐κB pathways .…”

Section: Discussionmentioning

confidence: 99%

Increased M1 macrophages in young miR‐15a/16^−/− mice with tumour grafts or dextran sulphate sodium‐induced colitis

Jia

Han

et al. 2018

Scand J Immunol

View full text Add to dashboard Cite

M1 macrophages are involved in inflammation by producing proinflammatory cytokines, whereas M2 macrophages are associated with wound healing and tissue regeneration by producing anti-inflammatory cytokines. MicroRNAs are involved in macrophage polarization. To evaluate whether miR-15a/16 is involved in macrophage polarization under tumour or inflammation microenvironments, we observed the growth of transplanted hepatic cancer (H22) cells or severity of dextran sulphate sodium (DSS)-induced colitis in 8-week-old miR-15a/16 knockout (KO) mice. Compared with littermate controls, the miR-15a/16 mice exhibited retarded tumour growth and increased sensibility to DSS-induced colitis. Meanwhile, the M1 cell frequencies were higher in tumour tissues and inflamed colons of KO mice than of littermate controls. Macrophages with miR-15a/16 deletion revealed an enhanced NF-κB transcription under the physiological state and lipopolysaccharide (LPS) or high mobility group box 1 (HMGB1) stimulation. STAT3 expression was also significantly increased in miR-15a/16 macrophages under LPS or HMGB1 stimulation. The polarization of M1 macrophages can be associated with the coactivation of NF-κB and STAT3. Results indicated that miR-15a/16 deficiency in the macrophages directs M1 polarization for tumour suppression and proinflammation. Thus, miR-15a/16 deletion in macrophages holds a distinct biological significance from that of the microRNA deficiency in tumour cells.

show abstract

Section: Discussionmentioning

confidence: 99%

Increased M1 macrophages in young miR‐15a/16^−/− mice with tumour grafts or dextran sulphate sodium‐induced colitis

Jia

Han

et al. 2018

Scand J Immunol

View full text Add to dashboard Cite

show abstract

“…SHH treatment upregulated the expression of iNOS and TNF-α mRNA ( Figure 2B). Activation of the NF-κB signaling pathway has been reported to induce M1 macrophage differentiation and the consequent inflammatory effects [14,21]. To establish if NF-κB activation is involved in the SHH-induced upregulation of iNOS and TNF-α mRNA expression, the NF-κB inhibitor BAY11-7085 was combined with SHH treatment.…”

Section: Reduction Of Il-4-induced M2 Polarization In Mouse Peritoneamentioning

confidence: 99%

Sea Hare Hydrolysate-Induced Reduction of Human Non-Small Cell Lung Cancer Cell Growth through Regulation of Macrophage Polarization and Non-Apoptotic Regulated Cell Death Pathways

Nyiramana

Cho

Kim

et al. 2020

Cancers

View full text Add to dashboard Cite

Sea hare-derived compounds induce macrophage activation and reduce asthmatic parameters in mouse models of allergic asthma. These findings led us to study the role of sea hare hydrolysates (SHH) in cancer pathophysiology. SHH treatment-induced M1 macrophage activation in RAW264.7 cells, peritoneal macrophages, and THP-1 cells, as did lipopolysaccharide (LPS) (+ INF-γ), whereas SHH reduced interleukin (IL)-4 (+IL-13)-induced M2 macrophage polarization. In addition, SHH treatment inhibited the actions of M1 and M2 macrophages, which have anticancer and pro-cancer effects, respectively, in non-small cell lung cancer cells (A549 and HCC-366) and tumor-associated macrophages (TAMs). Furthermore, SHH induced G2/M phase arrest and cell death in A549 cells. SHH also downregulated STAT3 activation in macrophages and A549 cells, and the down-regulation was recovered by colivelin, a STAT3 activator. SHH-induced reduction of M2 polarization and tumor growth was blocked by colivelin treatment. SHH-induced cell death did not occur in the manner of apoptotic signaling pathways, while the death pattern was mediated through pyroptosis/necroptosis, which causes membrane rupture, formation of vacuoles and bleb, activation of caspase-1, and secretion of IL-1β in SHH-treated A549 cells. However, a combination of SHH and colivelin blocked caspase-1 activation. Z-YVAD-FMK and necrostatin-1, pyrotosis and necroptosis inhibitors, attenuated SHH's effect on the cell viability of A549 cells. Taken together, SHH showed Cancers 2020, 12, 726 2 of 24 anticancer effects through a cytotoxic effect on A549 cells and a regulatory effect on macrophages in A549 cells. In addition, the SHH-induced anticancer effects were mediated by non-apoptotic regulated cell death pathways under STAT3 inhibition. These results suggest that SHH may be offered as a potential remedy for cancer immunotherapy.

show abstract

“…Previous studies found that polyporus polysaccharide (PPS) could alleviate the adverse reactions of Bacille Calmette-Guerin BCG and improve its e ciency [12], and effectively inhibit the progression of N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN)-induced bladder cancer in rats [13]. In the following study, PPS was found to increase the expression level of CD86 and CD40 in bladder cancer tissue of rats [12], and regulate the immune activity of macrophages and promoted them to M1-like macrophages [14]. Therefore, it was speculated that PPS inhibited the progression of bladder cancer by regulating macrophage polarization in tumor macroenvironment.…”

Section: Introductionmentioning

confidence: 77%

Polyporus polysaccharide regulates proliferation, apoptosis and migration of bladder cancer cells by polarizing macrophages to M1 subtype in tumor microenvironment

Jia¹,

Luo²,

Lai³

et al. 2020

Preprint

Self Cite

View full text Add to dashboard Cite

Background: Polyporus polysaccharide (PPS), an active ingredient of traditional Chinese medicinal Polyporus umbellatus, has multiple biological functions, such as anti-cancer, immune-regulating and hepatoprotective activities. The purpose of this study was to investigate the mechanism of PPS activated macrophages in the treatment of bladder cancer.Methods: 100 ng/mL Phorbol myristate acetate (PMA) was used to induce THP-1 human leukemic cells as a macrophage model. Flow cytometry was used to detect the expression of CD14 and CD68 to verify the establishment of macrophage model. After that, Macrophages derived from THP-1 were treated with different concentrations of PPS (1,10 and 100 ug/mL). Flow cytometry and RT-PCR were used to detected the expression of CD16, CD23, CD86, CD40 and interleukin (IL)-Iβ, iNOS mRNA. ELISA was used to test the change of IL-1β and TNF-α in macrophage after the treatment with PPS. The conditioned medium from PPS-polarized macrophages was used to detect the effect of activated macrophages on bladder cancer. MTT assay, 5-ethynyl-2¢-deoxyuridine assay, flow cytometry, Transwell assay, and Western blot analysis were used to detect the effects of polarized macrophages on the viability, proliferation, apoptosis, and migration of bladder cancer cells. Western blot was also used to analysis the change of JAK2/NF-κB pathway protein.Results: PPS promoted the expression of pro-inflammatory factors, such as IL-Iβ, TNF-α and iNOS, and surface molecules CD86, CD16, CD23, and CD40 in macrophages and then polarized macrophages to M1 type. The results demonstrated that activated macrophages inhibited the proliferation of bladder cancer cells, regulated their apoptosis, and inhibited migration and epithelial–mesenchymal transformation (EMT). JAK2/NF-κB pathways were downregulated in the anti-bladder cancer process of activated macrophages. Conclusion: The findings indicated that PPS inhibited the proliferation and progression of bladder cancer by the polarization of macrophages to M1 type, and JAK2/NF-κB pathway was downregulated in the process of anti-bladder cancer.

show abstract

NF-κB pathways are involved in M1 polarization of RAW 264.7 macrophage by polyporus polysaccharide in the tumor microenvironment

Cited by 91 publications

References 33 publications

Increased M1 macrophages in young miR‐15a/16^−/− mice with tumour grafts or dextran sulphate sodium‐induced colitis

Increased M1 macrophages in young miR‐15a/16^−/− mice with tumour grafts or dextran sulphate sodium‐induced colitis

Sea Hare Hydrolysate-Induced Reduction of Human Non-Small Cell Lung Cancer Cell Growth through Regulation of Macrophage Polarization and Non-Apoptotic Regulated Cell Death Pathways

Polyporus polysaccharide regulates proliferation, apoptosis and migration of bladder cancer cells by polarizing macrophages to M1 subtype in tumor microenvironment

Contact Info

Product

Resources

About

NF-κB pathways are involved in M1 polarization of RAW 264.7 macrophage by polyporus polysaccharide in the tumor microenvironment

Cited by 91 publications

References 33 publications

Increased M1 macrophages in young miR‐15a/16−/− mice with tumour grafts or dextran sulphate sodium‐induced colitis

Increased M1 macrophages in young miR‐15a/16−/− mice with tumour grafts or dextran sulphate sodium‐induced colitis

Sea Hare Hydrolysate-Induced Reduction of Human Non-Small Cell Lung Cancer Cell Growth through Regulation of Macrophage Polarization and Non-Apoptotic Regulated Cell Death Pathways

Polyporus polysaccharide regulates proliferation, apoptosis and migration of bladder cancer cells by polarizing macrophages to M1 subtype in tumor microenvironment

Contact Info

Product

Resources

About

Increased M1 macrophages in young miR‐15a/16^−/− mice with tumour grafts or dextran sulphate sodium‐induced colitis

Increased M1 macrophages in young miR‐15a/16^−/− mice with tumour grafts or dextran sulphate sodium‐induced colitis