Shichao Han

Safety and efficacy of radical hysterectomy based on embryo development-originated in the treatment of early cervical cancer: a single-arm meta-analysis

Cervical cancer is the leading malignancy in terms of both incidence and mortality among cancers of the female reproductive system, and initial surgical treatment is still one of the main treatments. However, for many years, radical hysterectomy based on traditional anatomical principles has failed to substantially improve oncological outcomes for cervical cancer patients or reduce the incidence of perioperative complications. In recent years, radical surgery grounded in the membrane anatomy concept of embryonic development has demonstrated promising oncological outcomes in colorectal cancer surgery. Research in the field of cervical cancer, however, remains in its early stages, although it is steadily garnering increased attention. Consequently, this meta-analysis seeks to systematically assess the safety and efficacy of radical hysterectomy, rooted in embryonic developmental principles, for the treatment of early-stage cervical cancer. This study systematically searched PubMed, Embase, Cochrane Library, Web of Science, Wanfang, and CNKI databases for relevant studies published from their inception to October 2024. Data on 5-year recurrence-free survival (RFS), overall survival (OS), and surgical complications were collected for further analysis. Eight studies involving 1,226 patients were included in the meta-analysis. The surgical complication rate was 35.2%. Two studies reported a 5-year RFS of 86% and an OS of 88%. Radical hysterectomy based on embryo development-originated shows good safety and efficacy in treating early-stage cervical cancer. PROSPERO Identifier: CRD42024602098.

DARS-AS1 Knockdown Inhibits the Growth of Cervical Cancer Cells via Downregulating HMGB1 via Sponging miR-188-5p

Background: Evidence has been shown that long noncoding RNAs (lncRNAs) play an important role in the development of cervical cancer. Recently, lncRNA DARS-AS1 was shown to be dysregulated in several cancer types, but the role of DARS-AS1 in cervical cancer remains unclear. Methods: Immunofluorescence staining, flow cytometry and transwell invasion assays were used to determine proliferation, apoptosis and invasion in cervical cancer cells, respectively. The dual luciferase reporter system assay was performed to assess the interaction between DARS-AS1, miR-188-5p, and high mobility group box 1 (HMGB1) in cervical cancer cells. Results: Downregulation of DARS-AS1 markedly inhibited the proliferation and invasion of cervical cancer cells. Moreover, DARS-AS1 knockdown obviously induced the apoptosis of SiHa and HeLa cells. Meanwhile, luciferase reporter assay identified that miR-188-5p was the potential miRNA binding of DARS-AS1, and HMGB1 was the potential binding target of miR-188-5p. Mechanistic analysis indicated that downregulation of DARS-AS1 decreased the expression of HMGB1 by acting as a competitive “sponge” of miR-188-5p. Conclusion: In this study, we found that DARS-AS1 knockdown suppressed the growth of cervical cancer cells via downregulating HMGB1 via sponging miR-188-5p. Therefore, DARS-AS1 might serve as a potential target for the treatment of cervical cancer.

Histone deacetylase 10 exerts antitumor effects on cervical cancer via a novel microRNA‐223/TXNIP/Wnt/β‐catenin pathway

AbstractDysfunction of histone deacetylase 10 (HDAC10) has been suggested in the carcinogenesis of cervical cancer (CC). However, its association with microRNAs (miRNAs) in CC remains exclusive. Hence, this study aims to probe the role of HDAC10 in regulating CC cell proliferation, migration, and invasion and its correlation with the screened‐out miRNA target. Microarray analysis and RT‐qPCR revealed that HDAC10 expressed poorly in CC cells relative to human immortalized endocervical cells (End1/E6E7). Moreover, HDAC10 downregulation predicted poor survival for patients with CC. Overexpression of HDAC10 reduced CC cell biological activities in vitro and tumor growth and lung metastases in vivo. miR‐223, upregulated in CC, was regulated by HDAC10 through histone acetylation, while miR‐223 inhibited the effects of HDAC10 overexpression in CC. miR‐223 targeted the 3′‐UTR of thioredoxin interacting protein (TXNIP) and suppressed its expression, leading to increased CC development in vitro and in vivo. TXNIP overexpression impaired Wnt/β‐catenin pathway activity in CC cells.