Rong Li

Enhancing Sonodynamic Therapy for Cervical Cancer Using Ultrasound-Activated BTO@PEG

Patients with advanced cervical cancer have a poor prognosis, and sonodynamic therapy (SDT) is expected to offer a new approach for improving the therapeutic outcome of cervical cancer due to its noninvasiveness and ability to penetrate deeply into tissues. In order to overcome the problems of the rapid elimination and low water solubility of organic acoustic sensitizers in SDT, DSPE-PEG

Constitutive expression of progesterone receptor isoforms promotes the development of hormone-dependent ovarian neoplasms

Altering the relative abundance of progesterone receptor isoforms drives ovarian neoplasia in mice.

LncRNA HCG11 represses ovarian cancer cell growth via AKT signaling pathway

AbstractAimOvarian cancer is a main contributor of cancer‐relevant deaths among women worldwide due to high incidence and mortality. Mounting evidence has unveiled that lncRNAs play critical roles in malignancies, including ovarian cancer. Although the tumor suppressor function of HCG11 in prostate cancer and glioma has been proved, investigations on HCG11 role in ovarian cancer are still scarce.MethodsGene or protein expression was quantified by RT‐qPCR or western blot. HCG11 effects on ovarian cancer were assessed by functional assays. Bioinformatics analysis and mechanism experiments were implemented to identify the association among HCG11, miR‐1270, and PTEN.ResultsHCG11 was weakly expressed in ovarian cancer and functioned as a tumor suppressor in ovarian cancer by retarding cell proliferation, migration, and EMT. Besides, HCG11 could bind to miR‐1270 and PTEN was a target gene of miR‐1270. Mechanically, HCG11 competitively bound with miR‐1270 to upregulate PTEN. From rescue experiments, HCG11 impeded AKT/mTOR pathway to retard ovarian cancer cell growth by miR‐1270/PTEN.ConclusionsHCG11 was a tumor suppressor in ovarian cancer cells and additionally, HCG11 regulated AKT/mTOR pathway to hinder ovarian cancer cell growth via modulating miR‐1270/PTEN, indicating that HCG11 may represent a promising target for effective treatment of ovarian cancer patients.

Expression and correlation analysis of Skp2 and CBX7 in cervical cancer

Aims S-phase kinase-associated protein 2 (Skp2) oncoprotein is overexpressed in a variety of cancer tissues and promotes the malignant development of cancer. The expression levels of chromobox homolog 7 (CBX7) protein are varied among different types of cancer tissues, but its role in cervical cancer is not clear. We aimed to examine the expression and clinical significance of Skp2 and CBX7 proteins as well as their correlations in cervical cancer. Methods Immunohistochemistry was used to detect the expression of Skp2 and CBX7 proteins in the cancerous tissues and adjacent tissues of 64 patients with cervical cancer. Relevant clinicopathological data of these patients were collected, compared and analysed for the correlations. Results The expression of Skp2 protein in cervical cancer (87.5%) was higher than that in paracancerous tissues (14.1%), and the expression was positively correlated with clinical stage, malignant degree, lymphatic metastasis, vascular invasion and interstitial invasion. The expression of CBX7 protein in cervical cancer (48.4%) was lower than that in paracancerous tissues (96.8%), and the expression was negatively correlated with clinical stage, malignant degree, interstitial invasion, vascular invasion and lymphatic metastasis. The expression of Skp2 protein and CBX7 protein in cervical cancer tissues and adjacent tissues was negatively correlated. The expression of Skp2 and CBX7 proteins was closely related to the clinicopathological features of cervical cancer. Conclusions CBX7 may play the role of a tumour suppressor gene in cervical cancer and provide reference value for the diagnosis and new targeted treatment of cervical cancer.

Guttate psoriasis induced by interferon alfa‐2b suppository treatment for high‐grade cervical intraepithelial neoplasia

MIG-6 Regulates HDAC1-Mediated Angiogenesis and Tumorigenesis in PTEN-Deficient Endometrioid Endometrial Cancer

Abstract Endometrioid endometrial cancer (EEC) is the most prevalent gynecologic malignancy, yet no targeted therapies are currently approved by the FDA specifically for it. To identify therapeutic targets for EEC, we performed transcriptomic and proteomic analyses in genetically engineered preclinical cancer models, including uterine-specific phosphatase and tensin homolog (Pten)-deficient (Ptend/d) mice and Ptend/d mice with additional overexpression of the tumor suppressor mitogen-inducible gene 6 (Mig-6) that develop EEC. Transcriptomic analysis revealed significant inhibition of immune, inflammatory, and angiogenesis pathways, with hypoxia-inducible factor-1α (HIF1α) as a key upstream regulator. Interactome and immunoprecipitation analyses identified HDAC1 as a MIG-6–interacting protein that mediates angiogenic signaling in PTEN-deficient endometrial cancer. MIG-6 overexpression suppressed HDAC1 activity and downstream HIF1α-driven angiogenesis. Pharmacologic inhibition of HDAC1 with panobinostat recapitulated the tumor-suppressive effects observed with MIG-6 overexpression. These findings suggest that HDAC1 may represent a potential therapeutic target in EEC and that HDAC inhibition can attenuate early tumor progression and angiogenic signaling in preclinical models. Implications: This study identifies the MIG-6–HDAC1 axis as a key regulator of angiogenesis in EEC, highlighting HDAC1 inhibition as a promising targeted therapeutic strategy for early tumor suppression.