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长链非编码 RNA HOXA11 反义 RNA 通过抑制 microRNA-518a 上调丝氨酸丰富蛋白 2 样来增强喉鳞状细胞癌对顺铂的耐药性。

Long non-coding RNA HOXA11 antisense RNA upregulates spermatogenesis-associated serine-rich 2-like to enhance cisplatin resistance in laryngeal squamous cell carcinoma by suppressing microRNA-518a.

机构信息

The Department of Otolaryngology Head and Neck Surgery, Tianjin Children's Hospital, Tianjin, China.

The Department of Otolaryngology Head and Neck Surgery, Affiliated Hospital of Hebei Engineering University, Handan, Hebei, China.

出版信息

Bioengineered. 2022 Jan;13(1):974-984. doi: 10.1080/21655979.2021.2016038.

DOI:10.1080/21655979.2021.2016038
PMID:34974809
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8805888/
Abstract

Long noncoding RNAs (LncRNAs) are closely associated with the chemoresistance of laryngeal squamous cell carcinoma (LSCC). Previous studies indicated that HOXA11-AS could function as a vital regulator in human cancers. However, the regulatory mechanisms of HOXA11-AS in the chemoresistance of LSCC remain unclear. In this study, it was found that HOXA11-AS expression was upregulated in cisplatin (CDDP)-resistant LSCC tissues and cells. Loss-of-function assays revealed that HOXA11-AS knockdown inhibited the viability, migration, and invasion, but promoted the apoptosis of CDDP-resistant LSCC cells. Meanwhile, we identified miR-518a as a downstream gene of HOXA11-AS in LSCC, and miR-518a silencing reversed the promotive effect of HOXA11-AS knockdown on CDDP sensitivity of LSCC cells. In addition, miR-518a could inhibit spermatogenesis-associated serine-rich 2-like (SPATS2L) expression by direct interaction, and upregulation of SPATS2L abrogated the inhibitory effect of HOXA11-AS silencing or miR-518a overexpression on CDDP resistance of CDDP-resistant LSCC cells. In sum, our results demonstrated that HOXA11-AS enhanced CDDP resistance of LSCC via miR-518a/SPATS2L axis, which might offer novel therapeutic strategies for CDDP-resistant LSCC.

摘要

长链非编码 RNA（lncRNAs）与喉鳞状细胞癌（LSCC）的化疗耐药密切相关。先前的研究表明，HOXA11-AS 可以作为人类癌症中的重要调节因子发挥作用。然而，HOXA11-AS 在 LSCC 化疗耐药中的调节机制尚不清楚。在本研究中，发现 HOXA11-AS 在顺铂（CDDP）耐药 LSCC 组织和细胞中表达上调。功能丧失实验表明，HOXA11-AS 敲低抑制 CDDP 耐药 LSCC 细胞的活力、迁移和侵袭，但促进其凋亡。同时，我们鉴定出 HOXA11-AS 在 LSCC 中的下游基因是 miR-518a，并且 miR-518a 沉默逆转了 HOXA11-AS 敲低对 LSCC 细胞 CDDP 敏感性的促进作用。此外，miR-518a 可以通过直接相互作用抑制生精相关丝氨酸丰富 2 样（SPATS2L）的表达，而上调 SPATS2L 则消除了 HOXA11-AS 沉默或 miR-518a 过表达对 CDDP 耐药 LSCC 细胞 CDDP 耐药性的抑制作用。总之，我们的研究结果表明，HOXA11-AS 通过 miR-518a/SPATS2L 轴增强 LSCC 的 CDDP 耐药性，这可能为 CDDP 耐药 LSCC 提供新的治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2401/8805888/bb8fd289d16e/KBIE_A_2016038_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2401/8805888/6f8343027d3a/KBIE_A_2016038_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2401/8805888/b914d7a5ad26/KBIE_A_2016038_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2401/8805888/f47d6d4d8f78/KBIE_A_2016038_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2401/8805888/72a44e735df5/KBIE_A_2016038_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2401/8805888/6821487695d8/KBIE_A_2016038_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2401/8805888/bb8fd289d16e/KBIE_A_2016038_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2401/8805888/6f8343027d3a/KBIE_A_2016038_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2401/8805888/b914d7a5ad26/KBIE_A_2016038_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2401/8805888/f47d6d4d8f78/KBIE_A_2016038_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2401/8805888/72a44e735df5/KBIE_A_2016038_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2401/8805888/6821487695d8/KBIE_A_2016038_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2401/8805888/bb8fd289d16e/KBIE_A_2016038_F0006_OC.jpg

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