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Your search keyword '"Zhimei Sheng"' showing total 3 results
Start Over Author "Zhimei Sheng" Topic breast cancer
3 results on '"Zhimei Sheng"'

1. Tumor‐derived exosomal miR‐148b‐3p mediates M2 macrophage polarization via TSC2/mTORC1 to promote breast cancer migration and invasion

Author

Chong Hao, Zhimei Sheng, Wenhao Wang, Ruijun Feng, Yuanhang Zheng, Qinpei Xiao, and Baogang Zhang

Subjects
breast cancer, exosomes, macrophage polarization, miR‐148b‐3p, TSC2, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background Emerging evidence has revealed that tumor‐associated macrophages (TAMs) and exosomes play a crucial role in the microenvironment for tumor growth. However, the mechanisms through which exosomal miRNAs modulate TAMs and tumor development in breast cancer are not fully understood. Methods We constructed a macrophage model and an indirect coculture system consist of breast cancer cells and macrophages. Exosomes were isolated from BC cells culture supernatant and identified by transmission electron microscopy, Western blot and Nanosight LM10 system. The expression of miR‐148b‐3p in exosomes was determined by qRT‐PCR and the effect of exosomal miR‐148b‐3p on macrophage polarization was measured using qRT‐PCR and ELISA. The proliferation, migration and invasion of BC cells were estimated by EdU, wound healing assay and transwell assay. We employed bioinformatics, luciferase reporter assay and Western blot to identify the target gene of miR‐148b‐3p. Western blot was used to clarify the mechanism of exosomal miR‐148b‐3p mediated the crosstalk between BC cells and M2 macrophages. Results Cancer‐derived exosomes could induce M2 polarization of macrophages, which promoted the migration and invasion of breast cancer cells. We found that exosomal miR‐148b‐3p was overexpressed in breast cancer cell‐derived exosomes and correlated with lymph node metastasis, late tumor stage and worse prognosis. Upregulated miR‐148b‐3p expression in exosomes modulated macrophage polarization by targeting TSC2, which promoted the proliferation and might affect migration and invasion of breast cancer cells. Interestingly, we found that exosomal miR‐148b‐3p could induce M2 macrophage polarization via the TSC2/mTORC1 signaling pathway in breast cancer. Conclusion Overall, our study elucidated that miR‐148b‐3p could be transported by exosomes from breast cancer cells to surrounding macrophages and induced M2 polarization by targeting TSC2, providing novel insights for breast cancer therapy.

Published
2023
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2. Cancer-associated fibroblast-derived exosomal miR-18b promotes breast cancer invasion and metastasis by regulating TCEAL7

Author

Hongli Li, Ruijun Feng, Chonggao Yin, Yuanhang Zheng, Lihong Shi, Wenhao Wang, Zhimei Sheng, Chong Hao, Qinpei Xiao, Ziqian Yan, Baogang Zhang, and Hao Luo

Subjects
Cancer Research, Immunology, Cancer associated fibroblast, Breast Neoplasms, Snail, Exosome, Article, Metastasis, Mice, Cellular and Molecular Neuroscience, Breast cancer, Cancer-Associated Fibroblasts, Single-molecule biophysics, Downregulation and upregulation, biology.animal, microRNA, medicine, Animals, Humans, Neoplasm Invasiveness, Neoplasm Metastasis, biology, QH573-671, Nuclear Proteins, Cell Biology, medicine.disease, Microvesicles, MicroRNAs, Cancer research, Female, Cytology
Abstract

Studies have shown that cancer-associated fibroblasts (CAFs) play an irreplaceable role in the occurrence and development of tumors. Therefore, exploring the action and mechanism of CAFs on tumor cells is particularly important. In this study, we compared the effects of CAFs-derived exosomes and normal fibroblasts (NFs)-derived exosomes on breast cancer cells migration and invasion. The results showed that exosomes from both CAFs and NFs could enter into breast cancer cells and CAFs-derived exosomes had a more enhancing effect on breast cancer cells migration and invasion than NFs-derived exosomes. Furthermore, microRNA (miR)-18b was upregulated in CAFs-derived exosomes, and CAFs-derived exosomes miR-18b can promote breast cancer cell migration and metastasis by specifically binding to the 3′UTR of Transcription Elongation Factor A Like 7 (TCEAL7). The miR-18b-TCEAL7 pathway promotes nuclear Snail ectopic activation by activating nuclear factor-kappa B (NF-κB), thereby inducing epithelial-mesenchymal transition (EMT) and promoting cell invasion and metastasis. Moreover, CAFs-derived exosomes miR-18b could promote mouse xenograft model tumor metastasis. Overall, our findings suggest that CAFs-derived exosomes miR-18b promote nuclear Snail ectopic by targeting TCEAL7 to activate the NF-κB pathway, thereby inducing EMT, invasion, and metastasis of breast cancer. Targeting CAFs-derived exosome miR-18b may be a potential treatment option to overcome breast cancer progression.

Published
2021

3. Cancer-Associated Fibroblasts Exosomal miR-106a Promotes Breast Cancer Invasion and Metastasis by Down -regulation of TCEAL7

Author

Hongli Li, Ruijun Feng, Chonggao Yin, baogang zhang, Yuanhang Zheng, Hao Luo, Ziqian Yan, Qinpei Xiao, Zhimei Sheng, and Lihong Shi

Subjects
Breast cancer, Mir 106a, Downregulation and upregulation, business.industry, Cancer research, Cancer-Associated Fibroblasts, Medicine, business, medicine.disease, Metastasis
Abstract

Studies have shown that cancer-associated fibroblasts (CAFs) play an irreplaceable role in the occurrence and development of tumors. Therefore, exploring the action and mechanism of CAFs on tumor cells is particularly important for designing new and effective treatments and improving prognosis of tumors. For exosomes have been shown to play vital roles in intercellular communication, in this study, we compared the effects of CAFs-derived exosomes and NFs-derived exosomes on breast cancer cell proliferation, migration, and metastasis. The results showed that exosomes from both CAFs and NFs could enter into breast cancer cells and CAFs-derived exosomes had a more enhancing effect on breast cancer cell proliferation and invasion than NFs-derived exosomes. Furthermore, it was found that the expression levels of miR-106a in exosomes derived from CAFs were significantly up-regulated than that of NFs-derived exosomes and what’s more, in vitro and in vivo studies have shown that miR-106a can promote breast cancer cell proliferation, migration and metastasis by specifically binding to the 3'UTR of TCEAL7. It is inspiring to find that the miR-106a-TCEAL7 pathway promotes Snail nuclear ectopic activation by activating NF-κB, thereby inducing epithelial-mesenchymal transition and promoting cell proliferation and metastasis. Moreover, a mouse xenograft model confirmed that CAFs-derived exosomes miR-106a could promote tumor metastasis. The above data shows that CAFs-derived exosomes miR-106a promote Snail nuclear ectopic by targeting TCEAL7 to activate the NF-κB pathway, thereby inducing EMT, invasion and metastasis of breast cancer. Targeting CAFs-derived exosome miR-106a may be a potential treatment option to overcome breast cancer progression.

Published
2021

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