Abstract
Background Although the tumorigenesis of cervical cancer (CC) has been widely investigated and recognized, the study of the systematic impact of histone deacetylase 10 (HDAC10), microRNA, and downstream molecular mechanisms in CC is still limited. Herein, cervical cancer, precancer lesions, and normal cervical tissues were collected to test the expression level of HDAC10, miR-223, and EPB41L3. The mechanism of HDAC10, miR-223, and EPB41L3 was interpreted in cervical cancer cells after HDAC10, miR-223, or EPB41L3 expression was altered. Results HDAC10 was poorly expressed in cervical cancer and precancer lesions, while miR-223 was highly expressed in cervical cancer. HDAC10 bound to miR-223, and miR-223 targeted EPB41L3. HDAC10 depressed the invasion property and tumorigenesis of cervical cancer via downregulating miR-223 and subsequently targeting EPB41L3. Conclusion The study clarifies that HDAC10 inhibits cervical cancer by downregulating miR-223 and subsequently targeting EPB41L3 expression, which might provide a new insight for management upon cervical cancer and precancer lesions.
Highlights
The tumorigenesis of cervical cancer (CC) has been widely investigated and recognized, the study of the systematic impact of histone deacetylase 10 (HDAC10), microRNA, and downstream molecular mechanisms in CC is still limited
Histone acetylation is mediated by two kinds of enzymes: histone acetyl transferases (HATs) and histone deacetylases (HDACs) [7]. e histone deacetylase (HDAC) family of transcriptional corepressors, which have been central in the understanding, have emerged as important regulators of cancer biogenesis
Is result means that cervical scraping samples with more severity tended to express a lower level of HDAC10 (Figure 1(a)). e results manifested that the protein expression level of HDAC10 was low in cervical cancer tissues (Figures 1(a), 1(b), and 1(d), Figure S1) and cells (Figure 1(c))
Summary
The tumorigenesis of cervical cancer (CC) has been widely investigated and recognized, the study of the systematic impact of histone deacetylase 10 (HDAC10), microRNA, and downstream molecular mechanisms in CC is still limited. Cervical cancer, precancer lesions, and normal cervical tissues were collected to test the expression level of HDAC10, miR223, and EPB41L3. HDAC10 depressed the invasion property and tumorigenesis of cervical cancer via downregulating miR-223 and subsequently targeting EPB41L3. E study clarifies that HDAC10 inhibits cervical cancer by downregulating miR-223 and subsequently targeting EPB41L3 expression, which might provide a new insight for management upon cervical cancer and precancer lesions. While the multistage development of cancer biogenesis from cervical squamous intraepithelial lesion (SIL) to cancer was widely illustrated, the impact of posttranslational modifications of histone proteins on cervical cancer tumorigenic process is poorly understood.
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