Targeting transient receptor potential canonical 1 reduces non-small cell lung cancer chemoresistance and sternness via inhibition of PI3K/AKT signaling

Targeting transient receptor potential canonical 1 reduces non-small cell lung cancer chemoresistance and sternness via inhibition of PI3K/AKT signaling

TRPC1 enhances cell proliferation and migration in non-small cell lung cancer (NSCLC); however, its effect on NSCLC chemoresistance and sternness remains to be determined. The aim of the current study was to investigate the effect of TRPC1 on NSCLC chemoresistance and sternness and to determine the...

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Veröffentlicht in:Oncology letters 2023-08, Vol.25 (6), p.1
Hauptverfasser: Jin, Jiahui, Yan, Xinyu, Zhao, Yaru, Zhang, Haojie, Zhuang, Kai, Wen, Yating, He, Jingjing, Gao, Junzhen
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Cancer
Care and treatment
Lung cancer, Non-small cell
Lung cancer, Small cell
RNA
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container_issue 6
container_start_page 1
container_title Oncology letters
container_volume 25
creator Jin, Jiahui
Yan, Xinyu
Zhao, Yaru
Zhang, Haojie
Zhuang, Kai
Wen, Yating
He, Jingjing
Gao, Junzhen
description TRPC1 enhances cell proliferation and migration in non-small cell lung cancer (NSCLC); however, its effect on NSCLC chemoresistance and sternness remains to be determined. The aim of the current study was to investigate the effect of TRPC1 on NSCLC chemoresistance and sternness and to determine the underlying mechanism of action. Cisplatin-resistant A549 (A549/CDDP) and H460 (H460/CDDP) cells were first established and were then transfected with negative control small interfering (si)RNA (si-NC) or TRPC1 siRNA (si-TRPCl). Cells were then treated with 740 Y-P, a PI3K/Akt agonist. Subsequently, the sensitivity of A549/CDDP and H460/CDDP cells to CDDP was evaluated. Furthermore, the expression levels of CD133 and CD44, and sphere formation ability were also determined. The results showed that the half-maximal inhibitory concentration (I[C.sub.50]) of CDDP was significantly higher in A549/CDDP cells compared with A549 cells and in H460/CDDP cells compared with H460 cells. TRPC1 silencing decreased the I[C.sub.50] value of CDDP compared with the si-NC group in A549/CDDP (11.78 vs. 21.58 [micro]M; P
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The aim of the current study was to investigate the effect of TRPC1 on NSCLC chemoresistance and sternness and to determine the underlying mechanism of action. Cisplatin-resistant A549 (A549/CDDP) and H460 (H460/CDDP) cells were first established and were then transfected with negative control small interfering (si)RNA (si-NC) or TRPC1 siRNA (si-TRPCl). Cells were then treated with 740 Y-P, a PI3K/Akt agonist. Subsequently, the sensitivity of A549/CDDP and H460/CDDP cells to CDDP was evaluated. Furthermore, the expression levels of CD133 and CD44, and sphere formation ability were also determined. The results showed that the half-maximal inhibitory concentration (I[C.sub.50]) of CDDP was significantly higher in A549/CDDP cells compared with A549 cells and in H460/CDDP cells compared with H460 cells. TRPC1 silencing decreased the I[C.sub.50] value of CDDP compared with the si-NC group in A549/CDDP (11.78 vs. 21.58 [micro]M; P<0.01) and H460/CDDP (23.76 vs. 43.11 [micro]M; P<0.05) cells. Additionally, TRPC1 knockdown in both cell lines decreased the number of spheres formed compared with the si-NC group. Furthermore, compared with the si-NC group, A549/CDDP cells transfected with si-TRPCl exhibited decreased levels of both CD133 (P<0.01) and CD44 (P<0.05). However, only CD133 (P<0.05) was downregulated in TRPC1-depleted H460/CDDP cells compared with the si-NC group. In addition, TRPC1 knockdown repressed PI3K/AKT signaling compared with the si-NC group in both A549/CDDP and H460/CDDP cells (all P<0.05). Finally, cell treatment with 740 Y-P reversed the effect of TRPC1 knockdown on PI3K/AKT signaling, chemoresistance, and cancer sternness in A549/CDDP and H460/CDDP cells (all P<0.05). In conclusion, the results of the current study suggested that targeting TRPC1 could attenuate cancer sternness and chemoresistance via suppression of PI3K/AKT signaling in NSCLC.]]></description><identifier>ISSN: 1792-1074</identifier><identifier>DOI: 10.3892/ol.2023.13810</identifier><language>eng</language><publisher>Spandidos Publications</publisher><subject>Cancer ; Care and treatment ; Lung cancer, Non-small cell ; Lung cancer, Small cell ; RNA</subject><ispartof>Oncology letters, 2023-08, Vol.25 (6), p.1</ispartof><rights>COPYRIGHT 2023 Spandidos Publications</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids></links><search><creatorcontrib>Jin, Jiahui</creatorcontrib><creatorcontrib>Yan, Xinyu</creatorcontrib><creatorcontrib>Zhao, Yaru</creatorcontrib><creatorcontrib>Zhang, Haojie</creatorcontrib><creatorcontrib>Zhuang, Kai</creatorcontrib><creatorcontrib>Wen, Yating</creatorcontrib><creatorcontrib>He, Jingjing</creatorcontrib><creatorcontrib>Gao, Junzhen</creatorcontrib><title>Targeting transient receptor potential canonical 1 reduces non-small cell lung cancer chemoresistance and sternness via inhibition of PI3K/AKT signaling</title><title>Oncology letters</title><description><![CDATA[TRPC1 enhances cell proliferation and migration in non-small cell lung cancer (NSCLC); however, its effect on NSCLC chemoresistance and sternness remains to be determined. The aim of the current study was to investigate the effect of TRPC1 on NSCLC chemoresistance and sternness and to determine the underlying mechanism of action. Cisplatin-resistant A549 (A549/CDDP) and H460 (H460/CDDP) cells were first established and were then transfected with negative control small interfering (si)RNA (si-NC) or TRPC1 siRNA (si-TRPCl). Cells were then treated with 740 Y-P, a PI3K/Akt agonist. Subsequently, the sensitivity of A549/CDDP and H460/CDDP cells to CDDP was evaluated. Furthermore, the expression levels of CD133 and CD44, and sphere formation ability were also determined. The results showed that the half-maximal inhibitory concentration (I[C.sub.50]) of CDDP was significantly higher in A549/CDDP cells compared with A549 cells and in H460/CDDP cells compared with H460 cells. TRPC1 silencing decreased the I[C.sub.50] value of CDDP compared with the si-NC group in A549/CDDP (11.78 vs. 21.58 [micro]M; P<0.01) and H460/CDDP (23.76 vs. 43.11 [micro]M; P<0.05) cells. Additionally, TRPC1 knockdown in both cell lines decreased the number of spheres formed compared with the si-NC group. Furthermore, compared with the si-NC group, A549/CDDP cells transfected with si-TRPCl exhibited decreased levels of both CD133 (P<0.01) and CD44 (P<0.05). However, only CD133 (P<0.05) was downregulated in TRPC1-depleted H460/CDDP cells compared with the si-NC group. In addition, TRPC1 knockdown repressed PI3K/AKT signaling compared with the si-NC group in both A549/CDDP and H460/CDDP cells (all P<0.05). Finally, cell treatment with 740 Y-P reversed the effect of TRPC1 knockdown on PI3K/AKT signaling, chemoresistance, and cancer sternness in A549/CDDP and H460/CDDP cells (all P<0.05). In conclusion, the results of the current study suggested that targeting TRPC1 could attenuate cancer sternness and chemoresistance via suppression of PI3K/AKT signaling in NSCLC.]]></description><subject>Cancer</subject><subject>Care and treatment</subject><subject>Lung cancer, Non-small cell</subject><subject>Lung cancer, Small cell</subject><subject>RNA</subject><issn>1792-1074</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid/><recordid>eNqNkF1LwzAUhnuh4Ji79D4geNcuH23SXo7hx5igF_N6pOlpG0mT0WT-Fn-uGYpsIGoO5OM9z3lPOElyRXDGyorOnckopiwjrCT4LJkQUdGUYJFfJDPvX3FcBSdlySfJ-0aOHQRtOxRGab0GG9AICnbBjWjnQnxraZCS1lmt4o3EdLNX4FFUUj9IE7MQN7OPJpFTMCLVw-BG8NqHg4CkbZAPMFoL3qM3LZG2va510M4i16LnFVvPF-sN8rqz0sTvXCbnrTQeZl_nNHm5u90sH9LHp_vVcvGYdqTieSpUlZOSEV63JSsaBYyLuhCFIBizmhZNQ1vABeFQt5WqaykoyTmjNOcCA8vZNLn-9O2kga22rYtzUIP2arsQnOII539QBaUV5TmJVPYDFaOBQStnodVRP7H9X8FRh5ujgh6kCb13Zn-Yoz91_h38dvwA0Wmtvg</recordid><startdate>20230801</startdate><enddate>20230801</enddate><creator>Jin, Jiahui</creator><creator>Yan, Xinyu</creator><creator>Zhao, Yaru</creator><creator>Zhang, Haojie</creator><creator>Zhuang, Kai</creator><creator>Wen, Yating</creator><creator>He, Jingjing</creator><creator>Gao, Junzhen</creator><general>Spandidos Publications</general><scope/></search><sort><creationdate>20230801</creationdate><title>Targeting transient receptor potential canonical 1 reduces non-small cell lung cancer chemoresistance and sternness via inhibition of PI3K/AKT signaling</title><author>Jin, Jiahui ; Yan, Xinyu ; Zhao, Yaru ; Zhang, Haojie ; Zhuang, Kai ; Wen, Yating ; He, Jingjing ; Gao, Junzhen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-g1964-7c9418316bf835dce367b57571003b25dd2fe0516ebf9cbba721463224670e343</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Cancer</topic><topic>Care and treatment</topic><topic>Lung cancer, Non-small cell</topic><topic>Lung cancer, Small cell</topic><topic>RNA</topic><toplevel>online_resources</toplevel><creatorcontrib>Jin, Jiahui</creatorcontrib><creatorcontrib>Yan, Xinyu</creatorcontrib><creatorcontrib>Zhao, Yaru</creatorcontrib><creatorcontrib>Zhang, Haojie</creatorcontrib><creatorcontrib>Zhuang, Kai</creatorcontrib><creatorcontrib>Wen, Yating</creatorcontrib><creatorcontrib>He, Jingjing</creatorcontrib><creatorcontrib>Gao, Junzhen</creatorcontrib><jtitle>Oncology letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jin, Jiahui</au><au>Yan, Xinyu</au><au>Zhao, Yaru</au><au>Zhang, Haojie</au><au>Zhuang, Kai</au><au>Wen, Yating</au><au>He, Jingjing</au><au>Gao, Junzhen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Targeting transient receptor potential canonical 1 reduces non-small cell lung cancer chemoresistance and sternness via inhibition of PI3K/AKT signaling</atitle><jtitle>Oncology letters</jtitle><date>2023-08-01</date><risdate>2023</risdate><volume>25</volume><issue>6</issue><spage>1</spage><pages>1-</pages><issn>1792-1074</issn><abstract><![CDATA[TRPC1 enhances cell proliferation and migration in non-small cell lung cancer (NSCLC); however, its effect on NSCLC chemoresistance and sternness remains to be determined. The aim of the current study was to investigate the effect of TRPC1 on NSCLC chemoresistance and sternness and to determine the underlying mechanism of action. Cisplatin-resistant A549 (A549/CDDP) and H460 (H460/CDDP) cells were first established and were then transfected with negative control small interfering (si)RNA (si-NC) or TRPC1 siRNA (si-TRPCl). Cells were then treated with 740 Y-P, a PI3K/Akt agonist. Subsequently, the sensitivity of A549/CDDP and H460/CDDP cells to CDDP was evaluated. Furthermore, the expression levels of CD133 and CD44, and sphere formation ability were also determined. The results showed that the half-maximal inhibitory concentration (I[C.sub.50]) of CDDP was significantly higher in A549/CDDP cells compared with A549 cells and in H460/CDDP cells compared with H460 cells. TRPC1 silencing decreased the I[C.sub.50] value of CDDP compared with the si-NC group in A549/CDDP (11.78 vs. 21.58 [micro]M; P<0.01) and H460/CDDP (23.76 vs. 43.11 [micro]M; P<0.05) cells. Additionally, TRPC1 knockdown in both cell lines decreased the number of spheres formed compared with the si-NC group. Furthermore, compared with the si-NC group, A549/CDDP cells transfected with si-TRPCl exhibited decreased levels of both CD133 (P<0.01) and CD44 (P<0.05). However, only CD133 (P<0.05) was downregulated in TRPC1-depleted H460/CDDP cells compared with the si-NC group. In addition, TRPC1 knockdown repressed PI3K/AKT signaling compared with the si-NC group in both A549/CDDP and H460/CDDP cells (all P<0.05). Finally, cell treatment with 740 Y-P reversed the effect of TRPC1 knockdown on PI3K/AKT signaling, chemoresistance, and cancer sternness in A549/CDDP and H460/CDDP cells (all P<0.05). In conclusion, the results of the current study suggested that targeting TRPC1 could attenuate cancer sternness and chemoresistance via suppression of PI3K/AKT signaling in NSCLC.]]></abstract><pub>Spandidos Publications</pub><doi>10.3892/ol.2023.13810</doi></addata></record>
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subjects Cancer
Care and treatment
Lung cancer, Non-small cell
Lung cancer, Small cell
RNA
title Targeting transient receptor potential canonical 1 reduces non-small cell lung cancer chemoresistance and sternness via inhibition of PI3K/AKT signaling
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