Biliang Chen

Background: Heat shock factor 1 ( HSF1 ), the principal transcriptional regulator of cellular stress responses, has been exhibited to play a role in the progression of various human cancer types. However, the function of HSF1 in endometrial cancer (EC) has not yet been evaluated. Objective: This study examined the expression and role of HSF1 in EC. Methods: Immunohistochemistry was performed to explore HSF1 level in 135 endometrial tissue specimens. The relationship between HSF1 level and EC patients’ clinicopathological characteristics was analyzed. Quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR) and Western blotting were employed to explore HSF1 expression level in tissues in vitro . Small interfering RNA (siRNA) was employed to suppress HSF1 expression level. The invasion and migration capacities were evaluated using transwell and wound healing assays. Cell cycle arrest and apoptosis were assessed by flow cytometric analysis. Results: EC tissues exhibited higher HSF1 expression level compared with normal endometrial and atypical endometrial hyperplasia tissues. High HSF1 expression level was associated with histological grade, muscular invasion, lymph node metastasis, and estrogen receptor (ER) expression level in EC tissues and cells. Kaplan–Meier analysis indicated that EC patients with elevated HSF1 expression level had poorer overall survival. Knockdown of HSF1 in EC cells resulted in cell cycle arrest, increased apoptosis, and inhibited EC cell proliferation, invasion, and migration. Conclusion: The results demonstrated that HSF1 could function as an oncogene in EC. HSF1 could play a notable role in EC progression. HSF1 may be a potential molecular target for both the treatment and prognosis of patients with EC.

The incidence of endometrial cancer (EC) is rapidly increasing worldwide. The majority of endometrial cancers are diagnosed at an early stage and are associated with a good prognosis; however, patients with advanced‑stage EC have a poor prognosis and present with invasive metastasis. The mechanisms responsible for the invasion and metastasis of endometrial cancer remain unknown. Here, the present study aimed to examine the effects of O‑GlcNAcylation on the malignancy of EC and its association with Yes‑associated protein (YAP). It was found that the expression of O‑GlcNAc transferase (OGT) and O‑GlcNAcylation were increased in EC tissues; the decrease in O‑GlcNAcylation levels was found to lead to the decreased proliferation, migration and invasion of EC cells. Mass spectrometric analysis revealed that OGT knockdown reduced the O‑GlcNAcylation of YAP. Furthermore, it was found that the reduction in the O‑GlcNAcylation of YAP promoted its phosphorylation, which in turn inhibited the access of YAP to the nucleus and downstream target gene activation, demonstrating that the level of O‑GlcNAcylation affects the development of EC. On the whole, the findings of the present study indicate that YAP is a key molecule linking the O‑GlcNAcylation and Hippo pathways, which together regulate the progression of EC.

Liang C, et al. J Gynecol Oncol. 2022 Dec;34:e20. https://doi.org/10.3802/jgo.2023.34.e20

Background Uterus transplantation is the only treatment for absolute uterine factor infertility. Complex vascular anatomy, long operation time, and intraoperative injuries are the main factors that limit progress in uterus transplantation. Moreover, robot-assisted uterus transplantation is not popular at present due to technical difficulties, with only a few countries reporting success. Methods In this paper, we present the key technical points of robot-assisted uterine transplantation by analyzing and summarizing our surgical experience and other successful cases of robot-assisted uterine transplantation. This study provides an evidence-based reference for clinicians planning robot-assisted uterine transplantation procedures. Conclusion Minimally invasive technologies can shorten the operation time, reduce injuries, and contribute to analyzing the anatomy of complex blood vessels. Therefore, robot-assisted uterine transplantation is an important direction for the future of uterine transplantation, and the findings and procedures reported herein contribute to the standardization and promotion of robot-assisted uterine transplantation operations.

Exosomes have been associated with chemoresistance in various cancers, but such a role in ovarian cancer is not yet clear. Here, using in vitro cell-based and in vivo mouse model experiments, we show that downregulation of O-GlcNAcylation, a key post-translational protein modification, promotes exosome secretion. This increases exosome-mediated efflux of cisplatin from cancer cells resulting in chemoresistance. Mechanistically, our data indicate that downregulation of O-GlcNAclation transferase (OGT) reduces O-GlcNAclation of SNAP-23. Notably, O-GlcNAcylation of SNAP-23 is vital for regulating exosome release in ovarian cancer cells. Reduced O-GlcNAclation of SNAP-23 subsequently promotes the formation of soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex consisting of SNAP-23, VAMP8, and Stx4 proteins. This enhances exosome release causing chemoresistance by increasing the efflux of intracellular cisplatin.

To select specific binding peptides for imaging and detection of human ovarian cancer. The phage 12-mer peptide library was used to select specific phage clones to ovarian cancer cells. After four rounds of biopanning, the binding specificity of randomly selected phage clones to ovarian cancer cells was determined by enzyme-linked immunosorbent assay (ELISA). DNA sequencing and homology analysis were performed on specifically bound phages. The binding ability of the selected peptides to SKOV3 cells was confirmed by fluorescence microscopy and flow cytometry. After four rounds of optimized biological panning, phage recovery was 34-fold higher than that of the first round, and the specific phage clones bound to SKOV3 cells were significantly enriched. A total of 32 positive phage clones were preliminarily identified by ELISA from 54 randomly selected clones, and the positive rate was 59.3%. S36 was identified as the clone with best affinity to SKOV3 cells via fluorescence microscopy and flow cytometry. A representative clone of OSP2, S36 is expected to be an effective probe for diagnosis and treatment of ovarian cancer.