Background

M2 tumor-associated macrophages are closely related to the progression and prognosis of breast cancer (BCa), and could be regulated by long intergenic non-coding RNAs (lincRNAs). Moreover, the differential expression of lincRNAs affects tumor resistance. This study focused on the potential involvement and mechanism of LINC00337 in BCa.

Methods

The expression of LINC00337 in BCa was detected by bioinformatics analysis and RT-qPCR. Cell viability and proliferation were analyzed by cell counting kit-8 (CCK-8) and clone formation assay. BCa cells were treated with different concentrations of paclitaxel (PAX) to determine the chemotherapy resistance of LINC00337. Tumor formation assay, Western blot, ELISA and immunohistochemistry were performed to determine the relationship between LINC00337 and PAX in vivo. Macrophages were induced to M2-like polarization, and then functional experiments (CCK-8, wound healing) and molecular experiments (ELISA, RT-qPCR, Western blot) were used to verify the role of LINC00337.

Results

LINC00337 was up-regulated in BCa. High-expressed LINC00337 accelerated viability and proliferation of BCa cells, improved the resistance of BCa cells to PAX, and accelerated tumor growth. Overexpressed LINC00337 up-regulated the expressions of M2 macrophage markers and M-CSF, and reduced the level of GM-CSF. PAX significantly reduced the viability of BCa cells and down-regulated LINC00337. Furthermore, the successfully induced M2 type macrophages to promote BCa cell activity, migration and EMT protein expression, and LINC00337 enhanced the effect of M2 type macrophages. ShLINC00337 had the opposite effect to overexpressed LINC00337.

Conclusion

LINC00337 accelerated the malignant phenotype of BCa cells and promoted chemoresistance to paclitaxel through M2-like macrophages.

中文翻译：

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LINC00337通过募集M2肿瘤相关巨噬细胞诱导乳腺癌的肿瘤发展和对紫杉醇的化学抗性

背景

M2 肿瘤相关巨噬细胞与乳腺癌 (BCa) 的进展和预后密切相关，并且可能受长基因间非编码 RNA (lincRNAs) 的调控。此外，lincRNA 的差异表达会影响肿瘤耐药性。本研究侧重于 LINC00337 在 BCa 中的潜在参与和机制。

方法

通过生物信息学分析和RT-qPCR检测LINC00337在BCa中的表达。通过细胞计数试剂盒-8 (CCK-8) 和克隆形成试验分析细胞活力和增殖。用不同浓度的紫杉醇 (PAX) 处理 BCa 细胞以确定 LINC00337 的化疗耐药性。进行肿瘤形成测定、蛋白质印迹、ELISA和免疫组织化学以确定LINC00337和PAX之间的体内关系。将巨噬细胞诱导为 M2 样极化，然后通过功能实验（CCK-8，伤口愈合）和分子实验（ELISA、RT-qPCR、Western blot）验证 LINC00337 的作用。

结果

LINC00337 在 BCa 中上调。高表达的 LINC00337 加速了 BCa 细胞的活力和增殖，提高了 BCa 细胞对 PAX 的抵抗力，并加速了肿瘤的生长。过表达 LINC00337 上调 M2 巨噬细胞标志物和 M-CSF 的表达，并降低 GM-CSF 的水平。PAX 显着降低 BCa 细胞的活力并下调 LINC00337。此外，成功诱导M2型巨噬细胞促进BCa细胞活性、迁移和EMT蛋白表达，LINC00337增强了M2型巨噬细胞的作用。ShLINC00337 与过度表达的 LINC00337 具有相反的效果。

结论

LINC00337 加速了 BCa 细胞的恶性表型，并通过 M2 样巨噬细胞促进了对紫杉醇的化学抗性。