Correction

Correction: HGF and c-Met Participate in Paracrine Tumorigenic Pathways in Head and Neck Squamous Cell Cancer

After publication of this article (Clin Cancer Res 2009;15:3740–50), which was published in the June 1, 2009, issue of Clinical Cancer Research (1), it came to the authors' attention that there had been an inadvertent error made regarding the identity of the UM-22B cancer cell line. Cells used for the in vivo experiment (Fig. 5) that were thought to be squamous cell head and neck cancer cell line UM-22B were, in fact, a cell line derived from squamous cell cancer of the bladder. The authors then underwent a process of authentication of the UM-22B cell line using DNA fingerprinting and repeated experiments from published Figs. 3–5 with inhibitors of c-Met using authenticated UM-22B cells that were shown to express c-Met. The results are shown below, which verify that authenticated UM-22B cells are responsive to c-Met inhibitors SU11274 and PF-2341066 in regard to inhibition of IL-8 release, reduction of phospho-c-Met, phospho-MAPK, and phospho-Akt, reduction of wound closure, and inhibition of growth in vivo. Effects showed the same level of significance as in the published experiments. Although the relative sensitivity of the authenticated cells to PF-2341066 in these experiments differs from the previously reported data (in most cases the authenticated cells are actually more sensitive than in the published assays, including in the in vivo growth assay), the conclusion of the published paper that blocking c-Met may be clinically useful for the treatment of HNSCC is substantiated.

Repeated Figure 5.

PF-2341066 inhibits authenticated UM-22B tumor xenograft growth in nude mice. A, UM-22B cells (3 × 10⁶) were injected into nude mice on day 0. On day 10, tumors were measured and experimental treatment was initiated. PF-2341066 was administered by oral gavage at 12.5mg/kg/d. A 76.6% inhibition in tumor volume was observed by day 20 in the PF-2341066 group. **, P = 0.008, unpaired Student's t-test. B, representative H&E staining of tumor from control and PF-2341066 treated animals. C, TUNEL assay staining on representative control and PF-2341066 treated tumors. Quantitation of 5 distinct areas per tumor sample (n = 4 per experimental treatment) at 40× magnification. *, P < 0.05, unpaired Student's t-test.

Repeated Figure 3C.

SU11274 treatment inhibits HGF-induced IL-8 secretion by authenticated UM-22B cells. Cells were serum-deprived for 48 h prior to 2 h pretreatment with 2.5 μM SU11274 or vehicle control with or without stimulation with 50 ng/ml HGF for 1 h. Cell culture supernatant was removed and analyzed using ELISA. Values are means ± SE of 4 samples per treatment group. ***, P < 0.0001, ANOVA.

Repeated Figure 4.

PF-2341066 inhibits c-Met activation. A, HNSCC cells (authenticated UM-22B) were serum-starved for 48 h followed by treatment with increasing concentrations of PF-2341066 for 2 h and then stimulated with 50ng/mL HGF for 5 min. The expression of phosphorylated and total c-Met, AKT, and MAPK were examined by Western blot. B, authenticated HNSCC UM-22B cells were grown to confluence followed by scratch wound induction. Cells were then treated with a concentration range of PF-2341066 (0-5 μM) for 48 h in the presence of 1% serum. Wound closure was measured at 10× magnification and compared to baseline measurements. *, P < 0.05 versus control, one-way ANOVA followed by the post-hoc Tukey-Kramer multiple comparisons test. Values are means ± SE of 6-9 samples per treatment group.