Progranulin Regulates Inflammation and Tumor

Liu, Chunxiao; Li, Jiayi; Shi, Wenjing; Zhang, Liujia; Liu, Shuang; Lian, Yingcong; Liang, Shuai; Wang, Hongyan

doi:10.2174/1871523018666190724124214

Cited by 26 publications

(17 citation statements)

References 86 publications

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“…The results of overexpression, knockout and supplementary experiments showed that miR-1246 can target DYRK1A, regulate the GSK-3β-Wnt/β-catenin signaling pathway, and inhibit the EMT of breast cancer cells. In recent years, studies have found that PGRN plays important roles in the proliferation, drug resistance, migration, and invasion of breast cancer, ovarian cancer, liver cancer and other tumors (13,14,36). In addition, serum PGRN levels are related to the treatment, survival and progression of breast cancer.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-1246 suppresses the metastasis of breast cancer cells by targeting the DYRK1A/PGRN axis to prevent the epithelial-mesenchymal transition

et al. 2022

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Objective. Breast cancer is one of the most common malignant and highly heterogeneous tumors in women. MicroRNAs (miRNAs), such as miR-1246, play important roles in various types of malignant cancers, including triple-negative breast cancer (TNBC). However, the biological role of miR-1246 in TNBChas not yet been fully elucidated. In this study, we studied the role of miR-1246 in the occurrence and development of TNBC and its mechanism of action.Methods. Cell Counting Kit-8 (CCK-8), wound healing, and Transwell assays were performed to observe the effects of miR-1246 on TNBC cell proliferation, migration, and invasion, respectively. The expression of epithelial-mesenchymal transition (EMT) markers was detected by western blotting. Dual luciferase reporter assays were performed to determine whether DYRK1A is a novel target of miR-1246. In addition, an immunoprecipitation experiment was performed to verify the binding of DYRK1A to PGRN. Rescue experiments were performed to determine whether DYRK1A is a novel target of miR-1246 and whether miR-1246 suppresses the metastasis of breast cancer cells by targeting the DYRK1A/PGRN axis to prevent the epithelial-mesenchymal transition.Results. Our results show that miR-1246 suppresses the proliferation, migration, and invasion of TNBC cells and that DYRK1A is a novel target of miR-1246. MiR-1246 plays a suppressive role in the regulation of the EMT of TNBC cells by targeting DYRK1A. DYRK1A mediates the metastasis of triple-negative breast cancer via activation of the EMT. We identi ed PGRN as a novel DYRK1A-interacting protein. DYRK1A and PGRN act together to regulate the occurrence and development of breast cancer through miR-1246. Conclusion. miR-1246 attenuates TNBC cell invasion and the EMT by targeting the DYRK1A/PGRN axis.Our data suggest that miR-1246 may be used to develop novel early-stage diagnostic and therapeutic strategies for TNBC.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-1246 suppresses the metastasis of breast cancer cells by targeting the DYRK1A/PGRN axis to prevent the epithelial-mesenchymal transition

et al. 2022

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“…Mutated TNF-α can directly lead to cell canceration ( Yang et al, 2018 ). Meanwhile, IL-6, IL-8, IL-1β, and other inflammatory cytokines can promote tumor proliferation and the development of cervical cancer ( Schäfer et al, 2013 ; Liu et al, 2020 ). For example, IL-1β regulates the expression of CCL-2 by activating nuclear factor-κ-gene binding (NF-κB).…”

Section: The Driving Effects Of Microbiome On Cervical Cancermentioning

confidence: 99%

From Microbiome to Inflammation: The Key Drivers of Cervical Cancer

et al. 2021

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Cervical cancer is the third leading cause of cancer-related death worldwide. Microbes and hosts form a mutually beneficial symbiosis relationship, and various parts of the host body are microbial habitats. Microbes can trigger inflammation in certain parts of the host body, contributing to cervical cancer development. This article reviews the relationship between cervicovaginal microbes, inflammation and cervical cancer, and discusses the effect of some key cervical microbes on cervical cancer. Finally, probiotic therapy and immunotherapy are summarized.

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“…In this study, we showed that ICA treatment was significantly upregulated the spleen and thymus index, as well as the levels of ALB in U14 cervical cancer mouse models. Furthermore, several studies have shown that cytokines can have quite an interesting effect on tumor immunity [ 27 , 28 ]. IFN‑γ, a multifunctional small‑molecule soluble protein, is produced by monocytes and lymphocytes [ 29 ], which plays an important role in the antiviral, anti-proliferative, and anti-tumor in cervical cancer [ 30 ].…”

Section: Discussionmentioning

confidence: 99%

“…TNF‑α, a cytokine naturally synthesized by the macrophages that directly leads to the death of cancer cells [ 32 ]. Meanwhile, the inflammatory cytokines, such as IL-6, IL-8, and IL-1β can promote tumor proliferation and the occurrence and development of cervical cancer [ 28 ]. In our study, we showed that the expression levels of IFN‑γ, IL-2, and TNF‑α were higher in ICA-treated groups than in the CTX group to ameliorate the immune function of mice.…”

Section: Discussionmentioning

confidence: 99%

Influence of icariin on inflammation, apoptosis, invasion, and tumor immunity in cervical cancer by reducing the TLR4/MyD88/NF-κB and Wnt/β-catenin pathways

Yang

et al. 2021

Cancer Cell Int

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Background Cervical cancer is a type of the most common gynecology tumor in women of the whole world. Accumulating data have shown that icariin (ICA), a natural compound, has anti-cancer activity in different cancers, including cervical cancer. The study aimed to reveal the antitumor effects and the possible underlying mechanism of ICA in U14 tumor-bearing mice and SiHa cells. Methods The antitumor effects of ICA were investigated in vivo and in vitro. The expression of TLR4/MyD88/NF-κB and Wnt/β-catenin signaling pathways were evaluated. Results We found that ICA significantly suppressed tumor tissue growth and SiHa cells viability in a dose-dependent manner. Also, ICA enhanced the anti-tumor humoral immunity in vivo. Moreover, ICA significantly improved the composition of the microbiota in mice models. Additionally, the results clarified that ICA significantly inhibited the migration, invasion capacity, and expression levels of TGF-β1, TNF-α, IL-6, IL-17A, IL-10 in SiHa cells. Meanwhile, ICA was revealed to promote the apoptosis of cervical cancer cells by down-regulating Ki67, survivin, Bcl-2, c-Myc, and up-regulating P16, P53, Bax levels in vivo and in vitro. For the part of mechanism exploration, we showed that ICA inhibits the inflammation, proliferation, migration, and invasion, as well as promotes apoptosis and immunity in cervical cancer through impairment of TLR4/MyD88/NF-κB and Wnt/β-catenin pathways. Conclusions Taken together, ICA could be a potential supplementary agent for cervical cancer treatment.

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Progranulin Regulates Inflammation and Tumor

Cited by 26 publications

References 86 publications

MicroRNA-1246 suppresses the metastasis of breast cancer cells by targeting the DYRK1A/PGRN axis to prevent the epithelial-mesenchymal transition

MicroRNA-1246 suppresses the metastasis of breast cancer cells by targeting the DYRK1A/PGRN axis to prevent the epithelial-mesenchymal transition

From Microbiome to Inflammation: The Key Drivers of Cervical Cancer

Influence of icariin on inflammation, apoptosis, invasion, and tumor immunity in cervical cancer by reducing the TLR4/MyD88/NF-κB and Wnt/β-catenin pathways

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