Long noncoding RNA HULC contributes to paclitaxel resistance in ovarian cancer via miR-137/ITGB8 axis

Long noncoding RNA (lncRNA) highly upregulated in liver cancer (HULC) has been reported to be implicated in chemoresistance. However, the potential mechanism of HULC in paclitaxel (PTX)-resistant ovarian cancer (OC) remains undefined. The expression of RNAs and proteins was measured by quantitative...

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Autores principales:	Huang Bo, Wei Min, Hong Li
Formato:	article
Lenguaje:	EN
Publicado:	De Gruyter 2021
Materias:	lncrna hulc mir-137 itgb8 paclitaxel resistance ovarian cancer Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/30ee7840bb774a1cbfe8482413a8bcd2
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spelling	oai:doaj.org-article:30ee7840bb774a1cbfe8482413a8bcd22021-12-05T14:10:41ZLong noncoding RNA HULC contributes to paclitaxel resistance in ovarian cancer via miR-137/ITGB8 axis2391-541210.1515/biol-2021-0058https://doaj.org/article/30ee7840bb774a1cbfe8482413a8bcd22021-07-01T00:00:00Zhttps://doi.org/10.1515/biol-2021-0058https://doaj.org/toc/2391-5412Long noncoding RNA (lncRNA) highly upregulated in liver cancer (HULC) has been reported to be implicated in chemoresistance. However, the potential mechanism of HULC in paclitaxel (PTX)-resistant ovarian cancer (OC) remains undefined. The expression of RNAs and proteins was measured by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and Western blot assay. The PTX resistance and apoptotic rate were assessed via 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry, respectively. Furthermore, the interaction between miR-137 and HULC or integrin beta-8 (ITGB8) was predicted by miRcode and starBase v2.0 and then verified by dual luciferase reporter and RNA pull-down assays. In addition, the xenograft mice model was established to explore the effects of HULC in vivo. HULC was significantly upregulated and miR-137 was downregulated in PTX-resistant OC tissues and cells. Also, the HULC depletion suppressed tumor growth and PTX resistance in PTX-treated mice. miR-137 was verified as a target of HULC and directly targeted ITGB8. And HULC knockdown downregulated ITGB8 expression by targeting miR-137. miR-137 inhibitor or ITGB8 overexpression mitigated the suppressive impacts of HULC knockdown on PTX resistance. Collectively, HULC modulated ITGB8 expression to promote PTX resistance of OC by sponging miR-137.Huang BoWei MinHong LiDe Gruyterarticlelncrna hulcmir-137itgb8paclitaxel resistanceovarian cancerBiology (General)QH301-705.5ENOpen Life Sciences, Vol 16, Iss 1, Pp 667-681 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	lncrna hulc mir-137 itgb8 paclitaxel resistance ovarian cancer Biology (General) QH301-705.5
spellingShingle	lncrna hulc mir-137 itgb8 paclitaxel resistance ovarian cancer Biology (General) QH301-705.5 Huang Bo Wei Min Hong Li Long noncoding RNA HULC contributes to paclitaxel resistance in ovarian cancer via miR-137/ITGB8 axis
description	Long noncoding RNA (lncRNA) highly upregulated in liver cancer (HULC) has been reported to be implicated in chemoresistance. However, the potential mechanism of HULC in paclitaxel (PTX)-resistant ovarian cancer (OC) remains undefined. The expression of RNAs and proteins was measured by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and Western blot assay. The PTX resistance and apoptotic rate were assessed via 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry, respectively. Furthermore, the interaction between miR-137 and HULC or integrin beta-8 (ITGB8) was predicted by miRcode and starBase v2.0 and then verified by dual luciferase reporter and RNA pull-down assays. In addition, the xenograft mice model was established to explore the effects of HULC in vivo. HULC was significantly upregulated and miR-137 was downregulated in PTX-resistant OC tissues and cells. Also, the HULC depletion suppressed tumor growth and PTX resistance in PTX-treated mice. miR-137 was verified as a target of HULC and directly targeted ITGB8. And HULC knockdown downregulated ITGB8 expression by targeting miR-137. miR-137 inhibitor or ITGB8 overexpression mitigated the suppressive impacts of HULC knockdown on PTX resistance. Collectively, HULC modulated ITGB8 expression to promote PTX resistance of OC by sponging miR-137.
format	article
author	Huang Bo Wei Min Hong Li
author_facet	Huang Bo Wei Min Hong Li
author_sort	Huang Bo
title	Long noncoding RNA HULC contributes to paclitaxel resistance in ovarian cancer via miR-137/ITGB8 axis
title_short	Long noncoding RNA HULC contributes to paclitaxel resistance in ovarian cancer via miR-137/ITGB8 axis
title_full	Long noncoding RNA HULC contributes to paclitaxel resistance in ovarian cancer via miR-137/ITGB8 axis
title_fullStr	Long noncoding RNA HULC contributes to paclitaxel resistance in ovarian cancer via miR-137/ITGB8 axis
title_full_unstemmed	Long noncoding RNA HULC contributes to paclitaxel resistance in ovarian cancer via miR-137/ITGB8 axis
title_sort	long noncoding rna hulc contributes to paclitaxel resistance in ovarian cancer via mir-137/itgb8 axis
publisher	De Gruyter
publishDate	2021
url	https://doaj.org/article/30ee7840bb774a1cbfe8482413a8bcd2
work_keys_str_mv	AT huangbo longnoncodingrnahulccontributestopaclitaxelresistanceinovariancancerviamir137itgb8axis AT weimin longnoncodingrnahulccontributestopaclitaxelresistanceinovariancancerviamir137itgb8axis AT hongli longnoncodingrnahulccontributestopaclitaxelresistanceinovariancancerviamir137itgb8axis
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Long noncoding RNA HULC contributes to paclitaxel resistance in ovarian cancer via miR-137/ITGB8 axis

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