Coexpression of EGFR and HER2 has been associated with poor disease outcome, high rates of metastasis and resistance to conventional treatments in breast cancer.
Surgical specimens from 64 patients who had undergone surgery for squamous cell carcinoma of the mobile tongue were assessed using immunohistochemistry to investigate the expression of HA and EGFR in the primary tumours, and the data were then correlated to cervical metastasis and survival.
In conclusion, (i) constitutive activation of EGFR/Akt/mTOR pathway was present in defined subset of NSCLC; (ii) mTOR/S6K/rS6 axis is frequently activated in AC, and constitutively activated through Akt by EGFR mutation even in SCC; and (iii) mTOR and rS6 are possible determinants of nodal metastasis in SCC and AC, respectively.
In sum, our study indicated that EGFR and PKM2 directly interact and bind with each other to regulate the transcription of stemness-related genes and promote the stem-like phenotype, thus promoting invasion and metastasis.
RBM5 is involved in the suppression of epidermal growth factor receptor (EGFR) expression, thus preventing proliferation, angiogenesis, invasion, and metastasis of lung cancer.
By FISH (n = 26), seven (27%) cases were discordant: six cases showed a high-level of EGFR polysomy in the primary tumor but not in the metastasis and one case showed a high-level of EGFR polysomy in the metastasis but not in the primary sample (Pearson correlation coefficient = 0.52, P = 0.007).
Finally, TEM8-Fc, a recombinant fusion protein comprising the extracellular domain of human TEM8 linked to the Fc portion of human IgG1, efficiently abrogated the interaction between uPA and TEM8, blocked uPA-induced migration of HepG2 cells in vitro and inhibited the growth and metastasis of human MCF-7 xenografts in vivo. uPA, TEM8 and EGFR overexpression and ERK1/2 phosphorylation were found co-located on frozen cancer tissue sections.
Based on this review, the expression of EGFR, c-erbB-2, VEGF, or MMPs play important roles for tumor growth, invasion and metastasis in HNSCC. c-erbB receptors, MMPs and VEGF might aid the clinician in the selection of an appropriate therapy for individual patients and help to predict the prognosis of patients.
EGFR expression was positively correlated with nuclear grade (P = 0.001) and negatively correlated with the hormonal receptor oestrogen receptor (P = 0.005). pEGFR was positively related to the Akt pathway (P = 0.008) and appeared to participate in invasion and metastasis (uPAR, P = 0.049; MMP-14, P = 0.025; VEGFR-1/Flt-1, P = 0.016).
Further analysis revealed that miR‑138 and miR‑204 were significantly downregulated in GC tissues and the overexpression of miR‑138 and miR‑204 in GC cell lines resulted in the significant inhibition of EGFR protein levels and GC cell proliferation and metastasis.
In ovarian cancer, the most lethal gynecological cancer, overexpression of the EGFR family is associated with more aggressive clinical behavior, increasing mortality rate caused by metastasis.
An association between high nEGFR expression and early recurrence was observed in patients with metastasis (HR[95% CI] =1.68[1.05~ 2.68], in progression-free survival).
Targeted tyrosine kinase inhibition can be considered in only a limited number of aggressive or metastatic tumors as EGFR, BRAF, or c-kit mutations are rare.
EGFR overexpression in the primary tumours was associated with lymph node progression, tumour-nodes-metastasis stage progression and proliferation (Ki-67 staining) in CSCC.
ROS1-rearranged tumors were also more likely to present with distant nodal metastases (ROS1, 15%; EGFR, 2%; P < .01) and sclerotic-type bone metastases (ROS1, 17%; EGFR, 6%; P < .01).
There is strong evidence demonstrating that activation of epidermal growth factor receptors (EGFRs) leads to tumor growth, progression, invasion and metastasis.