Abstract
Ovarian cancer is the most lethal gynecologic malignancy in the United States, with an estimated 22,530 new cases and 13,980 deaths in 2019. Recent studies have indicated that the phosphoinositol 3 kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR), as well as the nuclear factor-κ light chain enhancer of activated B cells (NFκB) pathways are highly mutated and/or hyper-activated in a majority of ovarian cancer patients, and are associated with advanced grade and stage disease and poor prognosis. In this review, we will investigate PI3K/AKT/mTOR and their interconnection with NFκB pathway in ovarian cancer cells.
Highlights
Ovarian cancer (OvCa) is the fifth most common type of cancer and the primary cause of gynecological cancer death in the United States [1]
The Cancer Genome Altas (TCGA) data revealed the hyperactivation of phosphoinositol 3 kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway in nearly 60% of patients with OvCa [1]
Several studies have reported that nearly 41% and 26.4% of high-grade serous cancer (HGSC) express the phosphorylated form of mTOR1 targets 4EBP1 and 70S6K, respectively, implying that mTORC1 activity is associated with a more aggressive phenotype and poor prognosis [126]
Summary
Ovarian cancer (OvCa) is the fifth most common type of cancer and the primary cause of gynecological cancer death in the United States [1]. The Cancer Genome Altas (TCGA) data revealed the hyperactivation of phosphoinositol 3 kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) (PI3K/AKT/mTOR) pathway in nearly 60% of patients with OvCa [1]. This pathway plays significant multifaceted roles in cancer cell growth, survival, metabolic programing, autophagy, transcription regulation, and angiogenesis [5,6,7]. The mutation profile of serous ovarian cystadenocarcinoma, generated from cBioPortal for Cancer Genomics (http://www.cbioportal.org/), indicates that several key players in the PI3K/AKT/mTOR/NFκB pathway are hyperactivated (Figure 1).
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
