In contrast, midkine (MK), a heparin-binding growth factor and cytokine, which induces carcinogenesis and chemoresistance, promotes the development and progression of many malignant tumours by increasing diverse cell functions such as cell proliferation, cell survival and antiapoptotic activities via mainly the activation of phosphatidyl inositol 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) pathways.
PI3K/AKT is an imperative pathway involved in theproliferation and tumorigenesis of cancer cells and herein it was found that Scopoletin could inhibit this pathway.
In addition, certain classical tumor pathways were also activated by target genes, among which, lncRNA MSTRG.1056.2 directly regulates ERBB3 to activate the PI3K-Akt pathway, contributing to tumorigenesis.
<b>Background:</b> Phosphatidylinositol 3-kinase (PI3K) pathway activation plays a key role in tumorigenesis and has been associated with poor prognosis and resistance to multiple therapies in various cancers.
Aberrant elevated PI3K activation has been reported to promote the tumorigenesis of breast cancer, but the mechanisms underlying are still needed to be elucidated.
Numerous signaling pathways, such as PI3K/Akt/mTOR and Wnt‑β‑catenin have been demonstrated to be associated with the tumorigenesis and development of RCC.
The review also brings forward the prospect of eIF4E to act as a converging juncture for signaling pathways like mTOR/PI3K and Mnk/MAPK to promote tumorigenesis.
The phosphoinositide 3-kinase (PI3K)/AKT/mechanistic target of rapamycin (mTOR) signaling has been shown to contribute to tumorigenesis, tumor progression, and resistance to therapy in most human cancer types, including lung cancer.
The aim of this review is to discuss the major miRNAs targeting proteins of the MAPK, PI3K, and TGFβ pathways, to define their mechanisms of action through the 3'UTR regions of their target genes, and to describe how they affect thyroid tumorigenesis through their actions on cell proliferation, migration, and invasion.
Comparing transcriptome profiles of human and mouse cell lines, miR-29b displayed common regulation pathways involving distinct downstream targets in macromolecular complex assembly, cell cycle regulation, and Wnt and PI3K-Akt signalling pathways; miR-29b also demonstrated specific functions reflecting cell characteristics, including fibrosis and neuronal regulations in NIH/3T3 cells and tumorigenesis and cellular senescence in HeLa cells.
Activation of phosphatidylinositol-3-kinase (PI3K) and downstream signalling by AKT/mammalian target of rapamycin (mTOR) modulates cellular processes such as increased cell growth, cell proliferation and increased cell migration as well as deregulated apoptosis and oncogenesis.
This study demonstrates that overexpression of CDCA2 might target CCND1 to promote CRC cell proliferation and tumorigenesis through activation of the PI3K/AKT pathway.
Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) is a tumor‑suppressor gene and can negatively regulate the phosphoinositide 3‑kinase (PI3K)/protein kinase B (Akt) signal transduction pathway, which is associated with cell proliferation, apoptosis and carcinogenesis.
We then determined whether fisetin and 5-FU together or singly affected tumorigenesis in Apc<sup>Min/+</sup> mice that also express constitutively active PI3K in the distal small intestine and colon.
Activating mutations in the catalytic subunit of Phosphatidylinositol (3,4,5)-trisphosphate kinase (PI3K), encoded by the <i>Pik3ca</i> gene, are detected in approximately 20% of human anal cancers.<b>Experimental Design:</b> We asked if common activating mutations in <i>Pik3ca</i> contribute to anal carcinogenesis using an established mouse model for anal carcinogenesis in which mice are topically treated with the chemical carcinogen 7,12-Dimethylbenz(a)anthracene (DMBA).
Phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway deregulation is closely associated with tumorigenesis.
The phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT), Mitogen-activated protein kinases (MAPK), and p53/p21 signal pathways play an important role in carcinogenesis, progression, and metastasis of carcinoma cells.