层状双氢氧化物负载si-NEAT1通过miR-133b/PD-L1轴调控乳腺癌紫杉醇耐药及巨噬细胞极化

doi:10.12122/j.issn.1673-4254.2025.08.16

南方医科大学学报 ›› 2025, Vol. 45 ›› Issue (8): 1718-1731.doi: 10.12122/j.issn.1673-4254.2025.08.16

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层状双氢氧化物负载si-NEAT1通过miR-133b/PD-L1轴调控乳腺癌紫杉醇耐药及巨噬细胞极化

张兆君¹(), 吴琼¹, 谢苗苗¹, 叶洳吟¹, 耿晨晨¹, 石纪雯¹, 杨清玲¹, 王文锐¹, 石玉荣²()

^1.蚌埠医科大学，安徽省肿瘤演进及智能诊疗重点实验室，安徽蚌埠 233030
^2.蚌埠医科大学，生物化学与分子生物学教研室，安徽蚌埠 233030

收稿日期:2024-12-24 出版日期:2025-08-20 发布日期:2025-09-05
通讯作者: 石玉荣 E-mail:zzj17318530948@163.com;shiyr@126.com
作者简介:张兆君，在读硕士研究生，E-mail: zzj17318530948@163.com
基金资助:
安徽省教育厅自然科学研究重点项目(KJ2021A0713);安徽省高校协同创新项目(GXXT-2022-064);安徽省高校优秀科研创新团队(2024AH010021);蚌埠医学院研究生科研创新项目(Byycxz23026);蚌埠医科大学研究生科研创新项目(Byycxz24018);蚌埠医科大学自然科学研究项目(2024 byzd050)

Layered double hydroxide-loaded si-NEAT1 regulates paclitaxel resistance and tumor-associated macrophage polarization in breast cancer by targeting miR-133b/PD-L1

Zhaojun ZHANG¹(), Qiong WU¹, Miaomiao XIE¹, Ruyin YE¹, Chenchen GENG¹, Jiwen SHI¹, Qingling YANG¹, Wenrui WANG¹, Yurong SHI²()

^1.Anhui Provincial Key Laboratory of Tumor Evolution and Intelligent Diagnosis and Treatment, Bengbu Medical University, Bengbu 233030, China
^2.Department of Biochemistry and Molecular Biology, Bengbu Medical University, Bengbu 233030, China

Received:2024-12-24 Online:2025-08-20 Published:2025-09-05
Contact: Yurong SHI E-mail:zzj17318530948@163.com;shiyr@126.com

摘要/Abstract

摘要：

目的研究层状双氢氧化物（LDH）负载si-NEAT1对乳腺癌紫杉醇耐药及肿瘤相关巨噬细胞极化作用的分子机制。方法 qRT-PCR、Western blotting检测乳腺癌亲本细胞（SKBR3）和紫杉醇耐药乳腺癌细胞（SKBR3-PR）中LncRNA NEAT1、miR-133b和PD-L1的表达；设置实验分组Control、si-NEAT1、miR-133b mimics，qRT-PCR、Western blotting检测SKBR3-PR中MRP、BCRP和PD-L1的表达，划痕、Transwell检测增殖迁移能力，流式细胞术检测细胞凋亡；采用si-NEAT1和miR-133b inhibitor进行Rescue实验；肿瘤细胞上清（CM）与巨噬细胞共培养，设置实验分组PBS、IL-4、PBS+SKBR3 CM、PBS+SKBR3-PR CM、IL-4+PR si-N CM，qRT-PCR检测M2型巨噬细胞标志物Arg-1、CD163、IL-10与miR-133b、PD-L1的表达，免疫荧光检测CD163与CD206；构建LDH@si-NEAT1纳米载体转染肿瘤细胞，设置分组Control、LDH、游离si-NEAT1、LDH@si-NEAT1，qRT-PCR、Western blotting、免疫荧光检测MRP、BCRP和PD-L1的表达，划痕、Transwell实验检测细胞增殖迁移能力，流式细胞术检测细胞凋亡；LDH@si-NEAT1 CM与巨噬细胞共培养，设置实验分组PBS、IL-4、IL-4+PR@ CM，qRT-PCR、免疫荧光检测Arg-1、CD163、IL-10及miR-133b和PD-L1的表达。结果相较于亲本乳腺癌细胞，紫杉醇耐药乳腺癌细胞中NEAT1表达上调、miR-133b下调和PD-L1上调（P<0.05）；si-NEAT1和 miR-133b mimics处理分别抑制了紫杉醇耐药乳腺癌细胞的活性，促进了细胞凋亡（P<0.01），MRP、BCRP表达下调（P<0.05）；敲低NEAT1，miR-133b表达上调，PD-L1表达下调（P<0.01），MRP、BCRP表达下调（P<0.001）；巨噬细胞M2型极化标志物Arg-1、CD163、IL-10在SKBR3-PR CM与巨噬细胞共培养后表达上调（P<0.05），而si-NEAT1 CM与巨噬细胞共培养后下调（P<0.05）；LDH@si-NEAT1作用肿瘤细胞，迁移侵袭能力下调，凋亡增加（P<0.01），MRP和BCRP以及PD-L1蛋白的表达降低（P<0.05），LDH@ si-NEAT1CM作用巨噬细胞Arg-1、CD163、IL-10表达下调，miR-133b上调，PD-L1下调（P<0.01）。结论 LDH@si-NEAT1通过靶向miR-133b/PD-L1轴，调控乳腺癌细胞紫杉醇耐药与巨噬细胞极化。

关键词: 乳腺癌紫杉醇耐药, 乳腺癌, LncRNA NEAT1, miR-133b, PD-L1, 层状双氢氧化物, M2型巨噬细胞极化

Abstract:

Objective To study the molecular mechanisms of LDH-loaded si-NEAT1 for regulating paclitaxel resistance and tumor-associated macrophage (TAM) polarization in breast cancer. Methods qRT-PCR and Western blotting were used to detect the expression of lncRNA NEAT1, miR-133b, and PD-L1 in breast cancer SKBR3 cells and paclitaxel-resistant SKBR3 cells (SKBR3-PR). The effects of transfection with si-NEAT1 and miR-133b mimics on MRP, MCRP and PD-L1 expressions and cell proliferation, migration and apoptosis were investigated using qRT-PCR, Western blotting, scratch and Transwell assays, and flow cytometry. Rescue experiments were conducted using si-NEAT1 and miR-133b inhibitor. Human THP-1 macrophages were cultured in the presence of conditioned media (CM) derived from SKBR3 and SKBR3-PR cells with or with si-NEAT1 transfection for comparison of IL-4-induced macrophage polarization by detecting the surface markers. LDH@si-NEAT1 nanocarriers were constructed, and their effects on MRP, MCRP and PD-L1 expressions and cell behaviors of the tumor cells were examined. THP-1 cells were treated with the CM from LDH@si-NEAT1-treated tumor cells, and the changes in their polarization were assessed. Results SKBR3-PR cells showered significantly upregulated NEAT1 and PD-L1 expressions and lowered miR-133b expression as compared with their parental cells. Transfection with si-NEAT1 and miR-133b mimics inhibited viability, promoted apoptosis and enhanced MRP and BCRP expressions in SKBR3-PR cells. NEAT1 knockdown obvious upregulated miR-133b and downregulated PD-L1, MRP and BCRP expressions. The CM from SKBR3-PR cells obviously promoted M2 polarization of THP-1 macrophages, which was significantly inhibited by CM from si-NEAT1-transfected cells. Treatment with LDH@si-NEAT1 effectively inhibited migration and invasion, promoted apoptosis, and reduced MRP, BCRP and PD-L1 expressions in the tumor cells. The CM from LDH@si-NEAT1-treated SKBR3-PR cells significantly downregulated Arg-1, CD163, IL-10, and PD-L1 and upregulated miR-133b expression in THP-1 macrophages. Conclusion LDH@si-NEAT1 reduces paclitaxel resistance of breast cancer cells and inhibits TAM polarization by targeting the miR-133b/PD-L1 axis.

Key words: paclitaxel resistance, breast cancer, lncRNA NEAT1, miR-133b, PD-L1, layered double hydroxide, M2 macrophage polarization

张兆君, 吴琼, 谢苗苗, 叶洳吟, 耿晨晨, 石纪雯, 杨清玲, 王文锐, 石玉荣. 层状双氢氧化物负载si-NEAT1通过miR-133b/PD-L1轴调控乳腺癌紫杉醇耐药及巨噬细胞极化[J]. 南方医科大学学报, 2025, 45(8): 1718-1731.

Zhaojun ZHANG, Qiong WU, Miaomiao XIE, Ruyin YE, Chenchen GENG, Jiwen SHI, Qingling YANG, Wenrui WANG, Yurong SHI. Layered double hydroxide-loaded si-NEAT1 regulates paclitaxel resistance and tumor-associated macrophage polarization in breast cancer by targeting miR-133b/PD-L1[J]. Journal of Southern Medical University, 2025, 45(8): 1718-1731.

图/表 11

表1 PCR引物序列表

Tab.1 PCR primer sequences

Gene	Forward primer	Reverse primer
GAPDH	CAGCCTCAAGATCATCAGCA	TGTGGTCATGAGTCCTTCCA
NEAT1	CTTCCTCCCTTTAACTTATCCATTCAC	CTCTTCCTCCACCATTACCAACAATAC
miR-133b	TCCCCTTCAACCAGCTAA	Universal primer
PD-L1	GTAAGACCACCACCACCAATTC	AGTTGTTGTGTTGATTCTCAGTGTG
U6	CTCGCTTCGGCAGCACA	AACGCTTCACGAATTTGCGT
Arg-1	GGACCTGCCCTTTGCTGACATC	TCTTCTTGACTTCTGCCACCTTGC
CD163	ACAATGAAGATGCTGGCGTGAC	ACAATGAAGATGCTGGCGTGAC
IL-10	ACCAAGACCCAGACATCAAGGC	AGGCATTCTTCACCTGCTCCAC
CD68	CCCACCTGCTTCTCTCATTCCC	TTGTACTCCACCGCCATGTAGC

图1 LncRNA NEAT1调控乳腺癌紫杉醇耐药

Fig.1 LncRNA NEAT1 regulates paclitaxel resistance of breast cancer cells. A, B: Western blotting and immunofluorescence detection of expression of drug resistance-related proteins in resistant breast cancer cells (scale bar=50 μm). C: qRT-PCR technology for detecting the expression of NEAT1. D: Western blotting for detecting drug resistance of the cells. E: Flow cytometry for analyzing apoptosis rate of the resistant breast cancer cells. F, G: Scratch and Transwell assays for assessing the migration and invasion capabilities of resistant cells (scale bar=200 μm). Scratch and Transwell assays for assessing migration and invasion capabilities of resistant breast cancer cells. *P<0.05, **P<0.01, ***P<0.001.

图2 LncRNA NEAT1通过调控miR-133b影响乳腺癌细胞耐药

Fig.2 LncRNA NEAT1 affects drug resistance in breast cancer cells by regulating miR-133b. A, B: qRT-PCR for detecting the expression of miR-133b. C: Western blotting for detecting expressions of drug resistance proteins. D: Immunofluorescence for detecting the expression of resistance proteins. E, F: Scratch and Transwell assays for assessing the migration and invasiveness of resistant cells. G: Flow cytometry for detecting apoptosis rate of resistant cells. *P<0.05, **P<0.01, ***P<0.001.

图3 LncRNA NEAT1调控miR-133b靶向PD-L1影响乳腺癌紫杉醇耐药

Fig.3 LncRNA NEAT1 regulates miR-133b to target PD-L1 and affect paclitaxel resistance in breast cancer cells. A, B: qRT-PCR for detecting the expression of PD-L1. C: Bioinformatics analysis reveals a regulatory relationship between miR-133b and PD-L1. D, E: Western blotting for detecting the expression of PD-L1. F: Western blotting for detecting the expressions of MRP, BCRP, and PD-L1 in drug-resistant breast cancer cells. *P<0.05, **P<0.01, ***P<0.001.

图4 LncRNA NEAT1通过调控miR-133b靶向PD-L1影响乳腺癌紫杉醇耐药

Fig.4 LncRNA NEAT1 regulates miR-133b to target PD-L1 and affect paclitaxel resistance in breast cancer cells. A: qRT-PCR for detecting the expression of PD-L1. B: Immunofluorescence for detecting the expression of BCRP in resistant cells (scale bar=50 μm). C, D: Scratch and Transwell assays for assessing migration and invasion capabilities of resistant cells (scale bar=200 μm). E: Flow cytometry for detecting apoptosis rate of the resistant cells. *P<0.05, **P<0.01, ***P<0.001.

图5 耐药细胞上清调控TAMs 极化

Fig.5 Resistance cell supernatant can regulate the polarization of tumor-associated macrophages. A: Morphology of Thp-1 and M0-type macrophages (scale bar=200 μm ). B: qRT-PCR for detecting the expression of CD68. C, D: qRT-PCR for detecting the expression of M2 macrophage polarization markers Arg-1, CD163, and IL-10. E: Immunofluorescence staining for detecting M2 polarization markers CD163 and CD206 in the macrophages (scale bar=50 μm). F: Timer2.0 website predicts that the expression of NEAT1 is positively correlated with macrophage infiltration. *P<0.05, **P<0.01, ***P<0.001.

图6 LncRNA NEAT1调控TAMs 极化

Fig.6 LncRNA NEAT1 regulates polarization of tumor-associated macrophages in breast cancer. A, D: qRT-PCR for detecting the expressions of NEAT1, miR-133b, and PD-L1, respectively. B, C: qRT-PCR and Immunofluorescence for detecting M2 macrophage polarization markers (scale bar=50 μm). E: Western blotting for detecting the expression of PD-L1 in the macrophages. *P<0.05, **P<0.01, ***P<0.001.

图7 LDH负载si-NEAT1纳米材料的构建

Fig.7 Construction of LDH Nanoparticles Loaded with si-NEAT1. A: Synthesis and loading of LDH. B: Agarose gel electrophoresis to determine the optimal loading ratio of LDH with si-NEAT1. C, D: Malvern particle size analysis for assessing particle size distribution and zeta potential of LDH and LDH@si-NEAT1. E: Transmission electron microscopy images of LDH and LDH@si-NEAT1. F, G: X-ray diffraction and UV-Vis spectra of LDH and LDH@si-NEAT1.

图8 表征LDH@ si-NEAT1实验

Fig.8 LDH@si-NEAT1 characterization experiments. A: Uptake experiment of LDH@si-NEAT1 (Original magnification: ×200). B: Confocal microscopy to detect lysosomal escape of LDH@si-NEAT1 (×200). C: Acridine orange staining to test lysosomal membrane permeability (×600).

图9 LDH@si-NEAT1调控乳腺癌细胞耐药

Fig.9 LDH@si-NEAT1 regulate paclitaxel resistance in breast cancer cells. A, B: Scratch and Transwell assays to assess the migration and invasion capabilities of drug-resistant cells. C: Flow cytometry for detecting apoptosis rate of drug-resistant cells. D: qRT-PCR for detecting expressions of miR-133b and PD-L1, respectively. E: Western blotting for detecting expressions of drug resistance proteins and PD-L1. *P<0.05, ***P<0.001.

图10 LDH@si-NEAT1调控巨噬细胞极化状态

Fig.10 LDH@si-NEAT1 regulate M2 polarization state. A: Immunofluorescence staining for detecting expressions of drug resistance proteins (scale bar=50 μm). B, C: qRT-PCR and immunofluorescence staining for detecting M2 macrophage polarization markers (scale bar=50 μm). D: qRT-PCR of the expressions of miR-133b and PD-L1. E: Western blotting of the expression of PD-L1 in macrophages. *P<0.05, **P<0.01, ***P<0.001.

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层状双氢氧化物负载si-NEAT1通过miR-133b/PD-L1轴调控乳腺癌紫杉醇耐药及巨噬细胞极化

Layered double hydroxide-loaded si-NEAT1 regulates paclitaxel resistance and tumor-associated macrophage polarization in breast cancer by targeting miR-133b/PD-L1

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