Additionally, a high level of TTN-AS1 in PTC was closely correlated with the activity of the phosphoinositide 3-kinase (PI3K)/Akt/mechanistic target of rapamycin (mTOR) pathway.
Whole exome sequencing (WES) recently identified frequent mutations in the genes of GPCR-mediated PI3K pathway (<i>LPAR4</i>, <i>PIK3CA</i>, and <i>PTEN</i>) in a Chinese population with papillary thyroid cancers (PTCs).
Finally, LINC00982 could regulate the activity of PI3K/AKT signaling pathway <i>in vitro</i> and <i>in vivo</i> Taken together, our findings demonstrated that overexpression of LINC00982 could suppress cell proliferation and induce cell apoptosis by regulating PI3K/AKT signaling pathway in PTC.
Overall, these findings indicated that miR‑766 may inhibit the malignant biological behaviors of PTC cells by directly targeting IRS2 and regulating the PI3K/Akt pathway, thus suggesting that this miRNA may be a promising therapeutic target for PTC.
Nine (69%) ATC cases with papillary thyroid carcinoma (PTC) components harboured BRAF mutations, all of which coexisted with a late mutation event (TP53, TERT, or PIK3CA).
In studying the expression of phosphoinositide-3 kinase (PI3K)/RAC serine/threonine-protein kinase (Akt) pathway, the upregulation of Ang1/Tie2 was found to be associated with the activation of the PI3K/Akt pathway in PTC.
Moreover, western blotting was used to show that the MAPK and PI3K-Akt pathways were aberrantly activated during <i>BANCR</i>-mediated PTC cell proliferation and migration.
Overexpression of miRNA‑148a significantly induced Bax protein expression and caspase‑3/9 levels, and suppressed phosphorylation STAT3 (p‑STAT3), PI3K and p‑Akt protein expression of papillary thyroid cancer in vitro.
We report PIK3CAE545K MF measurements in those tissues, as well as in normal breast, normal thyroid, mammary ductal carcinomas, and papillary thyroid carcinomas.
The results suggested that PIG3 plays an oncogenic role in PTC via the regulation of the PI3K/AKT/PTEN pathway and support the exploration of PIG3 as a novel biomarker for patients with PTC.
CXCR7 may regulate growth and metastasis of papillary thyroid carcinoma via the activation of PI3K/AKT pathway and its downstream NF-κB signaling, as well as the down-regulation of Notch signaling.
Tumors and matched normal thyroid samples were tested for RAS, for the v-raf murine sarcoma viral oncogene (BRAF) substitution of valine (V) for glutamate (E) at codon 600 (the V600E mutation), for phosphatase and tensin homolog (PTEN), for catalytic PI3k p110 subunit alpha (PIK3CA), for AKT, and for the presence of rearranged during transfection (ret) proto-oncogene/PTC (RET-PTC) and paired box-8 (PAX8)/peroxisome proliferator-activated receptor gamma (PPARgamma) fusion protein (PAX8-PPARgamma) rearrangements by direct sequencing and reverse transcriptase-polymerases chain reaction analyses, respectively.
It is proposed that genetic alterations in the PI3K/Akt pathway promote thyroid cell transformation to FTC and that genetic alterations in the MAPK pathway promote cell transformation to PTC; accumulation of multiple genetic alterations that can activate both pathways promotes thyroid cancer aggressiveness and progression to ATC.
PIK3CA amplification was seen in 265 of 499 PTC cases analyzed (53.1%); PIK3CA gene mutations in four of 207 PTC (1.9%); N2-RAS mutations in 16 of 265 PTC (6%); and BRAF mutations in 153 of 296 PTC (51.7%).
We found PIK3CA copy gain (defined as four or more copies) in nine of 31 FTC (29%), 20 of 141 PTC (14%), and five of 62 FTA (8%); PIK3CA gene mutations in four of 31 FTC (13%), one of 141 PTC (1%), and none of 62 FTA (0%); Ras mutations in three of 31 FTC (10%) and none of the 141 PTC and 62 FTA; and PTEN mutations in two of 31 FTC (6%) and none of 62 FTA (0%).
As to the three ATCs that had coexisted PTCs, mutated BRAF was detected in all PTC components but only in one ATC, while mutated PIK3CA was found in only one PTC component but not in the ATC.