Skip to main content
. Author manuscript; available in PMC: 2013 Jul 1.
Published in final edited form as: Cancer Genet. 2012 Jul;205(7-8):377–390. doi: 10.1016/j.cancergen.2012.05.001

Figure 1. Morphologic, genetic and functional description of the UOK268 cell line.

Figure 1

(A) Hematoxylin-eosin (H&E) staining of HLRCC kidney cancer removed surgically from the patients left renal tumor tissue (1X) and (B) H&E staining of tissue with 60X magnification to show consistent with atypical HLRCC pathological morphology: large nuclei with predominant nucleoli and atypical perinucleolar clearing.

(C) Genomic DNA mutation analysis revealed only germline mutant allele retained in UOK268 tumor cells.

(D) Western Blot analysis of the levels of HIF1α protein present in the lysates of UOK268, UOK262 and HK-2 cells. The expression levels of β–ACTIN were used as a loading control.

(E) Mutant FH protein is primarily localized to mitochondria of UOK268 cells shown by Alexa-Fluor®-488 labeling with a primary mouse monoclonal antibody to human FH. This overlaps almost completely with the signal from the Alexa-Fluor®-594 labeling with a primary rabbit polyclonal antibody to human mitochondrial protein SOD2.

(F) An In vitro assay of mutant FH enzyme activity from UOK268 tumor cell lysate was conducted by NADP-malic enzyme coupled assay and (G) as shown in Tong, et al,[12] the basal cellular respiration rate (oxygen consumption rate, OCR) of UOK268 and control cells was measured (here we use 786-O wt cell as positive control and UOK262 as negative control). OCR was normalized and shown as fMoles/min/cell.