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Background <p>Overexpression or downregulation of long noncoding RNA (lncRNA) plays an essential role in the progression and chemotherapy-resistant of breast cancer (BRCA). LncPRESS1 is a lncRNA regulated by p53, suggesting its potential in participating in carcinogenesis. However, few evidences reported the role of LncPRESS1 in tumor development.</p> Methods <p>The clinical significance of LncPRESS1 was explored in BRCA and normal samples derived from the patients. Overexpression and knockdown of LncPRESS1 were performed by lentivirus. CCK-8 and colony formation were conducted to examined the proliferation ability of BRCA cells. Apoptosis was measured by PI/Annexin V staining and the activity of caspase 3/7. Xenografted tumorigenesis in nude mice was applied to explore the role of LncPRESS1 on BRCA progression and cisplatin response. RT-qPCR was used to detect the mRNA level, while immunoblotting was applied to check the protein level.</p> Results <p>In this study, we identified that LncPRESS1 was significantly upregulated in BRCA tissues as compared with normal tissues, and in the cancer tissues with late stage or node metastasis. LncPRESS1 abundance was not changed among the patients based on the expression of estrogen receptor, progesterone receptor, or epidermal growth factor 2. In vitro, LncPRESS1 suppressed the apoptosis, while enhanced the proliferation and cisplatin resistance in BRCA cells. Upregulation of LncPRESS1 was also observed in the patients who did not response to cisplatin treatment. In vivo, knockdown of LncPRESS1 suppressed the tumorigenesis of BRCA cells and enhanced the effectiveness of cisplatin. Mechanistically, LncPRESS1 activated glycolysis via upregulation of ENO1. Overexpression of LncPRESS1 dictated the sensitivity of BRCA cells to ENO1 inhibitor, ENOblock. Importantly, treatment of ENOblock reduced the resistance of cisplatin in BRCA cells with overexpression of LncPRESS1.</p> Conclusion <p>In summary, we demonstrated that LncPRESS1 facilitated BRCA progression and cisplatin resistance via activation of ENO1-mediated glycolysis. Combination of ENO1 inhibitor and cisplatin was a promising therapeutic stragtegy for BRCA patients with overexpression of LncPRESS1.</p>

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LncPRESS1 promotes the progression and cisplatin resistance of breast cancer through upregulation of ENO1 and activation of glycolysis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月4日

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  • Longzhu Ke,
  • Wei Gao,
  • Yuanxiu Leng,
  • Jie Chen,
  • Hong Chen,
  • Shangshang Li,
  • Yingwen Zhang,
  • Li Luo

摘要

Background

Overexpression or downregulation of long noncoding RNA (lncRNA) plays an essential role in the progression and chemotherapy-resistant of breast cancer (BRCA). LncPRESS1 is a lncRNA regulated by p53, suggesting its potential in participating in carcinogenesis. However, few evidences reported the role of LncPRESS1 in tumor development.

Methods

The clinical significance of LncPRESS1 was explored in BRCA and normal samples derived from the patients. Overexpression and knockdown of LncPRESS1 were performed by lentivirus. CCK-8 and colony formation were conducted to examined the proliferation ability of BRCA cells. Apoptosis was measured by PI/Annexin V staining and the activity of caspase 3/7. Xenografted tumorigenesis in nude mice was applied to explore the role of LncPRESS1 on BRCA progression and cisplatin response. RT-qPCR was used to detect the mRNA level, while immunoblotting was applied to check the protein level.

Results

In this study, we identified that LncPRESS1 was significantly upregulated in BRCA tissues as compared with normal tissues, and in the cancer tissues with late stage or node metastasis. LncPRESS1 abundance was not changed among the patients based on the expression of estrogen receptor, progesterone receptor, or epidermal growth factor 2. In vitro, LncPRESS1 suppressed the apoptosis, while enhanced the proliferation and cisplatin resistance in BRCA cells. Upregulation of LncPRESS1 was also observed in the patients who did not response to cisplatin treatment. In vivo, knockdown of LncPRESS1 suppressed the tumorigenesis of BRCA cells and enhanced the effectiveness of cisplatin. Mechanistically, LncPRESS1 activated glycolysis via upregulation of ENO1. Overexpression of LncPRESS1 dictated the sensitivity of BRCA cells to ENO1 inhibitor, ENOblock. Importantly, treatment of ENOblock reduced the resistance of cisplatin in BRCA cells with overexpression of LncPRESS1.

Conclusion

In summary, we demonstrated that LncPRESS1 facilitated BRCA progression and cisplatin resistance via activation of ENO1-mediated glycolysis. Combination of ENO1 inhibitor and cisplatin was a promising therapeutic stragtegy for BRCA patients with overexpression of LncPRESS1.