Role of Phosphatidylinositol 3-Kinase and Its Catalytic Unit PIK3CA in Cervical Cancer: A Mini-Review

Abstract

In complicated disorders like cancer, signaling pathways form a tangled network. Targeting one gene may result in an unfavorable reaction from another off-target gene. Such entwined complexities may result in treatment resistance or failure in cancer patients. The PI3K/Akt/mTOR (phosphoinositol 3-kinase/protein kinase B/mammalian target of rapamycin) pathway is dysregulated in cervical cancer and is used as a biomarker for therapy. PI3K is a kinase that consists of a regulatory and catalytic domain and has phosphorylation capability. Class I components like the catalytic part (PIK3CA and PIK3CD) and regulatory part (like PIK3R1, PIK3R2, PIK3R3, and PIK3R5) are associated with oncogenesis and growth factors in cervical cancer. This review is aimed at discussing the involvement of the PI3K component of the PI3K/Akt/mTOR network in cervical cancer. Specifically, class I catalytic subunit PIK3CA has been identified as a pharmacological target, making it therapeutically significant. Apart from discussing the function of PI3K and PIK3CA in cervical cancer, we also discuss their inhibitors, which may be beneficial in treating cervical cancer.

Regulatory roles of Osteopontin in lung epithelial inflammation and epithelial‐telocyte interaction

“…We noticed that regulatory roles of OPN in PI3K subunit expression varied among changes, for example, PIK3CA, PIK3CB, PIK3R1, PIK3R2 and PIK3R3 were more sensitive to OPN when epithelia were challenged by CSE, PIK3CD and PIK3CD when challenged with CSE or LPS, as well as PIK3CA when challenged with the combination, respectively. Our data indicates that intra‐epithelial OPN strongly signals with PI3K class I components like the catalytic part (PIK3CA/p110α, PIK3CB/p110β, PIK3CD/p110δ and PIK3CG/p110γ) and regulatory part (PIK3R1, PIK3R2 and PIK3R3) in CSE‐induced epithelial origin inflammation, although those subunits may be involved in multiple biological processes 56,57 . Our results evidenced that external OPN‐induced epithelial origin interleukin production through PI3K/ERK signal pathways, although it remains unclear how those subunits coordinate and intercommunicate in OPN‐epithelial inflammation.…”

“…Our data indicates that intra-epithelial OPN strongly signals with PI3K class I components like the catalytic part (PIK3CA/p110α, PIK3CB/p110β, PIK3CD/p110δ and PIK3CG/p110γ) and regulatory part (PIK3R1, PIK3R2 and PIK3R3) in CSE-induced epithelial origin inflammation, although those subunits may be involved in multiple biological processes. 56,57 Our results evidenced that external OPN-induced epithelial origin interleukin production through PI3K/ERK signal pathways, although it remains unclear how those subunits coordinate and intercommunicate in OPN-epithelial inflammation. OPN could activate Akt/PKB and induce apoptosis by inhibiting the enzyme's ATP binding.…”

Multi-omic analysis of precocious puberty girls: pathway changes and metabolite validation

“…A study identified 16 unique variants of Gnai1 from 24 individuals, wherein the affected individuals suffered from severe neurodevelopmental disorders, including global developmental delay ( 40 ). Pik3r3 is a regulatory part of PI3K; dysregulated PI3K/Akt/mTOR in cervical cancer has been proved, and their inhibitors have been developed to treat cervical cancer ( 41 ). Some of these DEG-involved pathways were associated with PP, such as ovarian steroidogenesis, progesterone-mediated oocyte maturation, glycerolipid metabolism, fatty acid biosynthesis/degradation, arachidonic acid metabolism, and GnRH signaling pathway.…”

Retracted: Role of Phosphatidylinositol 3-Kinase and Its Catalytic Unit PIK3CA in Cervical Cancer: A Mini-Review

“…This article has been retracted by Hindawi following an investigation undertaken by the publisher [ 1 ]. This investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process: Discrepancies in scope Discrepancies in the description of the research reported Discrepancies between the availability of data and the research described Inappropriate citations Incoherent, meaningless and/or irrelevant content included in the article Peer-review manipulation …”

“…This article has been retracted by Hindawi following an investigation undertaken by the publisher [1]. This investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process:…”