Interestingly, Shh but not JAG2 was able to reduce beta-catenin signaling in SCC cells, arguing for a partial loss of negative feedback on beta-catenin transcription in tongue cancer.
The aim of the present study was to assess the anti-tumor effect of a defective adenovirus that expresses soluble vascular endothelial growth factor (VEGF) receptor FLT-1 (AdsFLT-1) in combination with cisplatin (cis-diamminedichloroplatinum, DDP) on human tongue carcinoma Tca8113 cell xenografts that had been pre-established in nude mice.
In the 51 clinical samples obtained from the patients with tongue carcinoma, the expression levels of phosphorylated (activated) form of Stat3 protein were significantly correlated with VEGF (P<0.05) production and intratumoral microvessel density IMVD (P<0.01).
Thus, the restoration of Pdcd4 levels by the use of molecular manipulation such as using a miR-155 sponge has an essential role in the therapeutic intervention of cancers, including tongue cancer.
Evidence indicates that in tongue cancer cells, FAM168A, also known as tongue cancer resistance-associated protein (TCRP1), can directly bind to AKT1 and regulate AKT1/NFκB signaling pathways.
To screen for additional treatment targets against tongue cancer, we evaluated the contributions of extracellular signal-related kinase (ERK), AKT and ezrin in cancer development.
Knockdown of Lnc‑EGFR inhibited the clonogenic ability and cell viability of human tongue cancer cell lines UM1 and CAL‑27, as evidenced by colony formation assays, and cell proliferation assays.
Knockdown of Lnc‑EGFR inhibited the clonogenic ability and cell viability of human tongue cancer cell lines UM1 and CAL‑27, as evidenced by colony formation assays, and cell proliferation assays.
Our results are of special importance against the background that CK19 positive carcinomas revealed a significantly poorer prognosis and therefore emphasize its prognostic and possible diagnostic role in tongue cancer.
Prior to monoculturing HSC-3tongue cancer cells, the model underwent modifications in oxygenation level (1%O2 hypoxia to upregulate CAV1) and/or in the amount of natural soluble factors [deleted by 14-day rinsing (rinsed myoma, RM), to allow only HSC-3-derived factors to act].
Identification of the ZEB1-CA9 signaling axis as a biomarker of poor prognosis in tongue cancer will be valuable in future development of therapeutic strategies aimed at improving treatment efficacy, especially in terms of drug resistance associated with this disease.
Carbonic anhydrase 9 (CA9) has been shown to be upregulated in the drug-resistant tongue cancer cell line Tca8113/PYM and to be associated with drug resistance.
The increased expression of pS(21)GSK3α and pS(9)GSK3β not only correlated positively with cyclin D1 and p53 expression in tongue cancer progression but a gradual shift of their expression from the cytoplasmic to the nuclear compartment and overall disease severity was also observed.
In this study, we investigated the effects and molecular mechanisms of miR-21 in chemosensitivity of tongue squamous cell carcinoma cells (TSCC) to cisplatin. miR-21 expression was detected in tongue cancer tissue using RT-PCR and PDCD4 protein expression was measured using immunohistochemistry. miR-21 and(or) PDCD4 depleted cell lines were generated using miR-21 inhibitor and(or) siRNA.
Tumor specimens and adjacent non-neoplastic tongue tissues from 74 patients with tongue carcinoma and human tongue carcinoma cell line Tca8113 were examined using immunohistochemistry and RT-PCR to determine the expressions of Notch1, Notch3, Jagged1, and Jagged2.
Interestingly, Shh but not JAG2 was able to reduce beta-catenin signaling in SCC cells, arguing for a partial loss of negative feedback on beta-catenin transcription in tongue cancer.