In conclusion, the results of the current study indicate that CACAN2D3 enhances the chemosensitivity of ESCC to cisplatin via inducing Ca<sup>2+</sup>-mediated apoptosis and suppressing PI3K/Akt pathways.
Functional enrichment analyses provided important clues to investigate the biological functions for SRCR gene network in ESCC, such as extracellular structure organization and the PI3K-Akt signaling pathway.
Collectively, our data suggests that JNK inhibition in combination with anti-PI3K therapy is a new therapeutic strategy that should be tested in HPVPos and HPVNeg HNSCC and ESCC patients.
Overexpression of miR-133b could suppress proliferation, migration and invasion of ESCC cells by inhibiting MAPK/ERK and PI3K/AKT signaling pathways through targeting EGFR, indicating that miR-133b might be a potential therapeutic target for the treatment of ESCC.
Our findings showed that circVRK1 suppressed ESCC progression by regulating miR-624-3p/PTEN axis and PI3K/AKT signaling pathway, suggesting the potential therapeutic value of circVRK1 for ESCC.
Upregulated miR-30b-5p may inhibit migration and invasion in ESCC by targeting ITGA5, PDGFRB, and signaling pathways, such as PI3K/Akt, involved in ESCC regulation.
<b>Conclusion:</b> Summarily, this study indicated that LSD1 might positively regulate Notch and PI3K/Akt/mTOR pathways through binding the promoter regions of related genes in Notch pathway in ESCC.
We found that ESCC cells harboring alterations in PI3K pathway were more resistant to radiation and combination of a clinical PI3Kα-selective inhibitor CYH33 and radiation synergistically inhibited cell proliferation in 14 ESCC cell lines.
In conclusion, our study showed that ACY-1215 suppressed proliferation and promoted apoptosis in ESCC via miR-30d/PI3K/AKT/mTOR and ERK pathways and that ACY-1215 may be a promising antitumor agent in ESCC.
Osthole inhibits the PI3K/AKT signaling pathway via activation of PTEN and induces cell cycle arrest and apoptosis in esophageal squamous cell carcinoma.
Moreover, we inactivated the PI3K pathway in ESCC cell lines with the PI3K inhibitor LY294002 and then detected STMN1 expression by western blot analysis.
The anti-tumor effects of dual PI3K/mTOR inhibitor BEZ235 and histone deacetylase inhibitor Trichostatin A on inducing autophagy in esophageal squamous cell carcinoma.
Lobaplatin promotes radiosensitivity, induces apoptosis, attenuates cancer stemness and inhibits proliferation through PI3K/AKT pathway in esophageal squamous cell carcinoma.
CONCLUSIONS The results indicated that CPS-C enhanced the anti-proliferative and apoptotic effect of oxaliplatin by modulating the PI3K/Akt/mTOR pathway on ESCC in vitro and in vivo.