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Qi Ling decreases paclitaxel resistance in the human prostate cancer by reversing tumor-associated macrophages function
Tumor-associated macrophages (TAMs) are critical immune cells infiltrated into tumor. In present study, we evaluated the effects of Qi Ling (QL), a traditional Chinese medicine on paclitaxel resistance in prostate cancer cells and explored the underlying mechanisms. We administrated QL to rats and c...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8908933/ https://www.ncbi.nlm.nih.gov/pubmed/35193986 http://dx.doi.org/10.18632/aging.203904 |
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author | Cao, Hongwen Wang, Dan Gao, Renjie Feng, Yigeng Chen, Lei |
author_facet | Cao, Hongwen Wang, Dan Gao, Renjie Feng, Yigeng Chen, Lei |
author_sort | Cao, Hongwen |
collection | PubMed |
description | Tumor-associated macrophages (TAMs) are critical immune cells infiltrated into tumor. In present study, we evaluated the effects of Qi Ling (QL), a traditional Chinese medicine on paclitaxel resistance in prostate cancer cells and explored the underlying mechanisms. We administrated QL to rats and collected the serum from QL-treated rats (QL-serum). We established the co-culture system of TAMs/paclitaxel resistant prostate cancer cells. We treated the TAMs with QL-serum and measured the viability of paclitaxel resistant prostate cancer cells after exposing to paclitaxel. We monitored the expression of M1 and M2 markers, the expression and activation of IL-6/STAT3 signaling pathways in TAMs after QL treatment. We treated TAMs with QL-serum together with interleukin (IL)-6, measured the expression of M1 and M2 markers, and the viability of paclitaxel resistant prostate cancer cells. In co-culture system, QL-serum-treated TAMs decreased the paclitaxel resistance in the human prostate cancer cells. QL-serum treatment significantly up-regulated the expression of M1 markers inducible nitric oxide synthase and tumor necrosis factor α while decreased the expression of M2 markers IL-10 and chemokine (C-C motif) ligand 22. QL-serum suppressed the activation of IL-6/ signal transducer and activator of transcription 3 signaling pathway. All these effects of QL-serum were abolished in the presence of IL-6. Qi Ling re-programmed TAMs and decreases paclitaxel resistance in prostate cancer cells. |
format | Online Article Text |
id | pubmed-8908933 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Impact Journals |
record_format | MEDLINE/PubMed |
spelling | pubmed-89089332022-03-11 Qi Ling decreases paclitaxel resistance in the human prostate cancer by reversing tumor-associated macrophages function Cao, Hongwen Wang, Dan Gao, Renjie Feng, Yigeng Chen, Lei Aging (Albany NY) Research Paper Tumor-associated macrophages (TAMs) are critical immune cells infiltrated into tumor. In present study, we evaluated the effects of Qi Ling (QL), a traditional Chinese medicine on paclitaxel resistance in prostate cancer cells and explored the underlying mechanisms. We administrated QL to rats and collected the serum from QL-treated rats (QL-serum). We established the co-culture system of TAMs/paclitaxel resistant prostate cancer cells. We treated the TAMs with QL-serum and measured the viability of paclitaxel resistant prostate cancer cells after exposing to paclitaxel. We monitored the expression of M1 and M2 markers, the expression and activation of IL-6/STAT3 signaling pathways in TAMs after QL treatment. We treated TAMs with QL-serum together with interleukin (IL)-6, measured the expression of M1 and M2 markers, and the viability of paclitaxel resistant prostate cancer cells. In co-culture system, QL-serum-treated TAMs decreased the paclitaxel resistance in the human prostate cancer cells. QL-serum treatment significantly up-regulated the expression of M1 markers inducible nitric oxide synthase and tumor necrosis factor α while decreased the expression of M2 markers IL-10 and chemokine (C-C motif) ligand 22. QL-serum suppressed the activation of IL-6/ signal transducer and activator of transcription 3 signaling pathway. All these effects of QL-serum were abolished in the presence of IL-6. Qi Ling re-programmed TAMs and decreases paclitaxel resistance in prostate cancer cells. Impact Journals 2022-02-22 /pmc/articles/PMC8908933/ /pubmed/35193986 http://dx.doi.org/10.18632/aging.203904 Text en Copyright: © 2022 Cao et al. https://creativecommons.org/licenses/by/3.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/3.0/) (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper Cao, Hongwen Wang, Dan Gao, Renjie Feng, Yigeng Chen, Lei Qi Ling decreases paclitaxel resistance in the human prostate cancer by reversing tumor-associated macrophages function |
title | Qi Ling decreases paclitaxel resistance in the human prostate cancer by reversing tumor-associated macrophages function |
title_full | Qi Ling decreases paclitaxel resistance in the human prostate cancer by reversing tumor-associated macrophages function |
title_fullStr | Qi Ling decreases paclitaxel resistance in the human prostate cancer by reversing tumor-associated macrophages function |
title_full_unstemmed | Qi Ling decreases paclitaxel resistance in the human prostate cancer by reversing tumor-associated macrophages function |
title_short | Qi Ling decreases paclitaxel resistance in the human prostate cancer by reversing tumor-associated macrophages function |
title_sort | qi ling decreases paclitaxel resistance in the human prostate cancer by reversing tumor-associated macrophages function |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8908933/ https://www.ncbi.nlm.nih.gov/pubmed/35193986 http://dx.doi.org/10.18632/aging.203904 |
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