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Low-dose paclitaxel downregulates MYC proto-oncogene bHLH transcription factor expression in colorectal carcinoma cells
Paclitaxel (PTX) has been commonly used to treat multiple types of tumor. Its anticancer mechanism differs based on different PTX concentrations and types of tumor cell. In the present study, MTT assays of HCT116 and LOVO cells treated with PTX revealed the chemosensitivity of the cell lines for dif...
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Published in: | Oncology Letters 2018, Vol.15 (2), p.1881 |
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container_title | Oncology Letters |
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creator | Li, Wenjing Zhu, Wanyun Lv, Chaoxiang Qu, Hao Xu, Kaixiang Li, Honghui Li, Haifeng Du, Yiming Liu, Guangming Wang, Yunyue Wei, Hong-Jiang Zhao, Hong-Ye |
description | Paclitaxel (PTX) has been commonly used to treat multiple types of tumor. Its anticancer mechanism differs based on different PTX concentrations and types of tumor cell. In the present study, MTT assays of HCT116 and LOVO cells treated with PTX revealed the chemosensitivity of the cell lines for different PTX concentrations. The half-maximal inhibitory concentration values of PTX for these cells were 2.46 and 2.24 nM, respectively. Cell morphology observation revealed that both cell lines exhibited rounded, wrinkled and damaged morphologies with increasing concentrations of PTX. Fluorescence-activated cell sorting analysis indicated that 1 nM PTX increased the proportion of cells in sub-[G.sub.1] phases and decreased the proportion of cells in [G.sub.0]/[G.sub.1] phases, whereas the proportions of cells in S and [G.sub.2]/M phases only slightly changed for both cell lines. Western blot analysis indicated that the total/nuclear protein expression of MYC proto-oncogene bHLH transcription factor (c-Myc) and phosphorylated (P)-c-Myc decreased in HCT116 cells in a dose-dependent manner, whereas the nuclear protein expression of P-c-Myc increased in LOVO cells in a dose-dependent manner. These results suggest that low-dose PTX downregulates c-Myc and P-c-Myc expression, subsequently inhibiting the cell cycle at [G.sub.0]/[G.sub.1] in colorectal carcinoma. Key words: paclitaxel, colorectal carcinoma cells, phosphorylated-MYC proto-oncogene bHLH transcription factor, cell cycle |
doi_str_mv | 10.3892/ol.2017.7525 |
format | report |
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Its anticancer mechanism differs based on different PTX concentrations and types of tumor cell. In the present study, MTT assays of HCT116 and LOVO cells treated with PTX revealed the chemosensitivity of the cell lines for different PTX concentrations. The half-maximal inhibitory concentration values of PTX for these cells were 2.46 and 2.24 nM, respectively. Cell morphology observation revealed that both cell lines exhibited rounded, wrinkled and damaged morphologies with increasing concentrations of PTX. Fluorescence-activated cell sorting analysis indicated that 1 nM PTX increased the proportion of cells in sub-[G.sub.1] phases and decreased the proportion of cells in [G.sub.0]/[G.sub.1] phases, whereas the proportions of cells in S and [G.sub.2]/M phases only slightly changed for both cell lines. Western blot analysis indicated that the total/nuclear protein expression of MYC proto-oncogene bHLH transcription factor (c-Myc) and phosphorylated (P)-c-Myc decreased in HCT116 cells in a dose-dependent manner, whereas the nuclear protein expression of P-c-Myc increased in LOVO cells in a dose-dependent manner. These results suggest that low-dose PTX downregulates c-Myc and P-c-Myc expression, subsequently inhibiting the cell cycle at [G.sub.0]/[G.sub.1] in colorectal carcinoma. Key words: paclitaxel, colorectal carcinoma cells, phosphorylated-MYC proto-oncogene bHLH transcription factor, cell cycle</description><identifier>ISSN: 1792-1074</identifier><identifier>DOI: 10.3892/ol.2017.7525</identifier><language>eng</language><publisher>Spandidos Publications</publisher><subject>Chemotherapy ; Colorectal cancer ; Development and progression ; Drug metabolism ; Drug therapy ; Genetic aspects ; Health aspects ; Paclitaxel ; Patient outcomes ; Transcription factors</subject><ispartof>Oncology Letters, 2018, Vol.15 (2), p.1881</ispartof><rights>COPYRIGHT 2018 Spandidos Publications</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail></links><search><creatorcontrib>Li, Wenjing</creatorcontrib><creatorcontrib>Zhu, Wanyun</creatorcontrib><creatorcontrib>Lv, Chaoxiang</creatorcontrib><creatorcontrib>Qu, Hao</creatorcontrib><creatorcontrib>Xu, Kaixiang</creatorcontrib><creatorcontrib>Li, Honghui</creatorcontrib><creatorcontrib>Li, Haifeng</creatorcontrib><creatorcontrib>Du, Yiming</creatorcontrib><creatorcontrib>Liu, Guangming</creatorcontrib><creatorcontrib>Wang, Yunyue</creatorcontrib><creatorcontrib>Wei, Hong-Jiang</creatorcontrib><creatorcontrib>Zhao, Hong-Ye</creatorcontrib><title>Low-dose paclitaxel downregulates MYC proto-oncogene bHLH transcription factor expression in colorectal carcinoma cells</title><title>Oncology Letters</title><description>Paclitaxel (PTX) has been commonly used to treat multiple types of tumor. Its anticancer mechanism differs based on different PTX concentrations and types of tumor cell. In the present study, MTT assays of HCT116 and LOVO cells treated with PTX revealed the chemosensitivity of the cell lines for different PTX concentrations. The half-maximal inhibitory concentration values of PTX for these cells were 2.46 and 2.24 nM, respectively. Cell morphology observation revealed that both cell lines exhibited rounded, wrinkled and damaged morphologies with increasing concentrations of PTX. Fluorescence-activated cell sorting analysis indicated that 1 nM PTX increased the proportion of cells in sub-[G.sub.1] phases and decreased the proportion of cells in [G.sub.0]/[G.sub.1] phases, whereas the proportions of cells in S and [G.sub.2]/M phases only slightly changed for both cell lines. Western blot analysis indicated that the total/nuclear protein expression of MYC proto-oncogene bHLH transcription factor (c-Myc) and phosphorylated (P)-c-Myc decreased in HCT116 cells in a dose-dependent manner, whereas the nuclear protein expression of P-c-Myc increased in LOVO cells in a dose-dependent manner. These results suggest that low-dose PTX downregulates c-Myc and P-c-Myc expression, subsequently inhibiting the cell cycle at [G.sub.0]/[G.sub.1] in colorectal carcinoma. Key words: paclitaxel, colorectal carcinoma cells, phosphorylated-MYC proto-oncogene bHLH transcription factor, cell cycle</description><subject>Chemotherapy</subject><subject>Colorectal cancer</subject><subject>Development and progression</subject><subject>Drug metabolism</subject><subject>Drug therapy</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Paclitaxel</subject><subject>Patient outcomes</subject><subject>Transcription factors</subject><issn>1792-1074</issn><fulltext>true</fulltext><rsrctype>report</rsrctype><creationdate>2018</creationdate><recordtype>report</recordtype><sourceid/><recordid>eNqVjEFOwzAQRb0AiQq64wBzgYTYbex0iSpQFmXHpitkJpPIaOqJbKP0-ASJC_Df4ktP-l-pR93Uu-5gnoRr02hXu9a0N2qj3cFUunH7O7XN-atZ01rddXajlpMs1SCZYPbIofgrMQyyxETTN_tCGd7OR5iTFKkkokwUCT77Uw8l-ZgxhbkEiTB6LJKArnOinH9NiIDCkgiLZ0CfMES5eEBizg_qdvScafvX96p-fXk_9tXkmT5CHGW9x5WBLgEl0hhW_9wa27nG7u3u34Mf6KlbSw</recordid><startdate>20180201</startdate><enddate>20180201</enddate><creator>Li, Wenjing</creator><creator>Zhu, Wanyun</creator><creator>Lv, Chaoxiang</creator><creator>Qu, Hao</creator><creator>Xu, Kaixiang</creator><creator>Li, Honghui</creator><creator>Li, Haifeng</creator><creator>Du, Yiming</creator><creator>Liu, Guangming</creator><creator>Wang, Yunyue</creator><creator>Wei, Hong-Jiang</creator><creator>Zhao, Hong-Ye</creator><general>Spandidos Publications</general><scope/></search><sort><creationdate>20180201</creationdate><title>Low-dose paclitaxel downregulates MYC proto-oncogene bHLH transcription factor expression in colorectal carcinoma cells</title><author>Li, Wenjing ; Zhu, Wanyun ; Lv, Chaoxiang ; Qu, Hao ; Xu, Kaixiang ; Li, Honghui ; Li, Haifeng ; Du, Yiming ; Liu, Guangming ; Wang, Yunyue ; Wei, Hong-Jiang ; Zhao, Hong-Ye</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-gale_infotracacademiconefile_A5268706463</frbrgroupid><rsrctype>reports</rsrctype><prefilter>reports</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Chemotherapy</topic><topic>Colorectal cancer</topic><topic>Development and progression</topic><topic>Drug metabolism</topic><topic>Drug therapy</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Paclitaxel</topic><topic>Patient outcomes</topic><topic>Transcription factors</topic><toplevel>online_resources</toplevel><creatorcontrib>Li, Wenjing</creatorcontrib><creatorcontrib>Zhu, Wanyun</creatorcontrib><creatorcontrib>Lv, Chaoxiang</creatorcontrib><creatorcontrib>Qu, Hao</creatorcontrib><creatorcontrib>Xu, Kaixiang</creatorcontrib><creatorcontrib>Li, Honghui</creatorcontrib><creatorcontrib>Li, Haifeng</creatorcontrib><creatorcontrib>Du, Yiming</creatorcontrib><creatorcontrib>Liu, Guangming</creatorcontrib><creatorcontrib>Wang, Yunyue</creatorcontrib><creatorcontrib>Wei, Hong-Jiang</creatorcontrib><creatorcontrib>Zhao, Hong-Ye</creatorcontrib></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Wenjing</au><au>Zhu, Wanyun</au><au>Lv, Chaoxiang</au><au>Qu, Hao</au><au>Xu, Kaixiang</au><au>Li, Honghui</au><au>Li, Haifeng</au><au>Du, Yiming</au><au>Liu, Guangming</au><au>Wang, Yunyue</au><au>Wei, Hong-Jiang</au><au>Zhao, Hong-Ye</au><format>book</format><genre>unknown</genre><ristype>RPRT</ristype><atitle>Low-dose paclitaxel downregulates MYC proto-oncogene bHLH transcription factor expression in colorectal carcinoma cells</atitle><jtitle>Oncology Letters</jtitle><date>2018-02-01</date><risdate>2018</risdate><volume>15</volume><issue>2</issue><spage>1881</spage><pages>1881-</pages><issn>1792-1074</issn><abstract>Paclitaxel (PTX) has been commonly used to treat multiple types of tumor. Its anticancer mechanism differs based on different PTX concentrations and types of tumor cell. In the present study, MTT assays of HCT116 and LOVO cells treated with PTX revealed the chemosensitivity of the cell lines for different PTX concentrations. The half-maximal inhibitory concentration values of PTX for these cells were 2.46 and 2.24 nM, respectively. Cell morphology observation revealed that both cell lines exhibited rounded, wrinkled and damaged morphologies with increasing concentrations of PTX. Fluorescence-activated cell sorting analysis indicated that 1 nM PTX increased the proportion of cells in sub-[G.sub.1] phases and decreased the proportion of cells in [G.sub.0]/[G.sub.1] phases, whereas the proportions of cells in S and [G.sub.2]/M phases only slightly changed for both cell lines. Western blot analysis indicated that the total/nuclear protein expression of MYC proto-oncogene bHLH transcription factor (c-Myc) and phosphorylated (P)-c-Myc decreased in HCT116 cells in a dose-dependent manner, whereas the nuclear protein expression of P-c-Myc increased in LOVO cells in a dose-dependent manner. These results suggest that low-dose PTX downregulates c-Myc and P-c-Myc expression, subsequently inhibiting the cell cycle at [G.sub.0]/[G.sub.1] in colorectal carcinoma. Key words: paclitaxel, colorectal carcinoma cells, phosphorylated-MYC proto-oncogene bHLH transcription factor, cell cycle</abstract><pub>Spandidos Publications</pub><doi>10.3892/ol.2017.7525</doi></addata></record> |
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source | PubMed Central |
subjects | Chemotherapy Colorectal cancer Development and progression Drug metabolism Drug therapy Genetic aspects Health aspects Paclitaxel Patient outcomes Transcription factors |
title | Low-dose paclitaxel downregulates MYC proto-oncogene bHLH transcription factor expression in colorectal carcinoma cells |
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