Exosomes, nano-sized extracellular vesicles for intercellular communications, are gaining rapid momentum as a novel strategy for the diagnosis and therapeutics of a spectrum of diseases including cancers. Secreted by various cell sources, exosomes pertain numerous functionalities from their parental cells and have enhanced stability that enable them with many features favorable for clinical use and commercialization. This paper focuses on the possible roles of exosomes in cancer therapeutics and reviews current exosome-based innovations toward enhanced cancer management and challenges that limit their clinical translation. Importantly, this paper casts insights on how cold atmospheric plasma, an emerging anticancer strategy, may aid in innovations on exosome-based onco-therapeutics toward improved control over cancers.

LncRNA SNHG7 shows a strong relationship with malignant behavior of cancer cells and poor clinical outcome in cancer. The resistance of ovarian cancer for Paclitaxel seriously limits the clinical efficacy in chemotherapy for ovarian cancer patients. In this study, we investigated whether lncRNA SNHG7 was involved in Paclitaxel sensitivity of ovarian cancer as well as the underlying mechanism regulating the behavior of ovarian cancer cells with Paclitaxel resistance. The experiment results of wound healing and transwell showed that in paclitaxel-resistant ovarian cancer cells, transfection with siRNA-SNHG7 in ovarian cancer cells reduced cell migration and invasion. And cell cycle was observed by means of Flow cytometry. RNA immunoprecipitation assay was performed to analyze the interaction of lncRNA SNHG7 and EIF4G2. Overexpression of EIF4G2 by transfection with Ov- EIF4G2 plasmids efficiently blocked the changes of migration and invasion, as well as G0/1 arrest caused by lncRNA SNHG7 silencing. Taken together, these results demonstrated that lncRNA SNHG7 could affect the degradation of EIF4G2 to regulate the sensitivity of ovarian cancer to Paclitaxel, inhibit cell viability, migration, and invasion. The interaction of lncRNA SNHG7 and EIF4G2 plays an important role in the migrative and invasive activity and Paclitaxel resistance of ovarian cancer cells.

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Ovarian cancer (OC) causes more deaths than any other cancer of the female reproductive system due to its late presentation and malignant nature. Although significant progress has been made in the diagnosis and treatment of OC over the last decade, chemotherapeutic drug resistance and cancer recurrence remain serious challenges in OC management. In the field of cancer therapy, traditional Chinese herbal medicines and their active compounds have been widely reported to have favorable therapeutic effects on cancer. Recent studies have also revealed the protective effect of puerarin in cancer, but the exact role and underlying mechanism of puerarin in OC remain unclear. Here, we established in vivo and in vitro OC models to evaluate the anticancer effect of puerarin. It was found that puerarin significantly inhibited OC cell viability and proliferation and induced cell apoptosis. In OC model mice, puerarin treatment suppressed tumor formation and modulated the gut microbiome. In addition, the expression of tumor suppressor genes was activated by puerarin in vitro and in vivo. These findings add to the existing knowledge on the usefulness of herbal active ingredients for the prevention and treatment of OC and provide a new perspective regarding the therapeutic potential of puerarin in cancer.

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the conversion of androgens to estrogens and progesterone synthesis [7]. Sadigh and others reported that the apoptotic and inflammation in the GC were related to the follicle, and the ovarian follicular growth was usually arrested in PCOS [8,9]. A clinical study reported that oxidative stress can induce the apoptosis of GCs in PCOS patients via the phosphoinositide 3-kinases/protein kinase B (PI3K/Akt) pathway [10]. Additional studies have demonstrated increased proliferation of GCs in the ovaries of anovulatory women compared to normal ovulatory women with PCOS [11]. Similarly, Ji found that the AT-rich interaction domain 1A (ARID1A) is downregulated in GC cells from women and in mouse models with PCOS, and the ARID1A overexpression can inhibit the PI3K/Akt pathway to

Objective: Puerarin has been proven to treat diverse cancers, but its function on ovarian cancer (OC) is still blurry and needs further research.Methods: After OC cells were treated with 10, 20, 40, 80, or 160 μg/mL pue, cell vitality, colony number, apoptosis, the positive expression of P53, migration, and invasion were examined by cell function experiments, TUNEL staining, and immunofluorescence. P53, P21, PTEN, FGF1, GLI2, and ERK1/2-NF-κB pathway-related marker expressions were examined by western blot. Results: Pue weakened the OC cell vitality, colony number, and the positive expression of P53 but enhanced apoptosis in a dose-dependent manner. Next, we discovered that pue enhanced the P53, P21, PTEN, and GLI2 levels but restrained the FGF1 level. Pue also alleviated the OC cell migration and invasion activity. We also confirmed that pue weakened the ERK1/2-NF-κB pathway-related marker expressions.Conclusion: Puerarin restrained the OC progression via modulating P53 and PTEN expressions.