Northern blot analysis of myeov gene expression in various tumor cell lines of human malignancy, a third-cycle mouse tumor (MA-T1A1) and NIH/3T3 recipient cells.

The purported or actual malignancy of the tumor cell lines are as follows: MCF-7, breast adenocarcinoma; HT-29, colon adenocarcinoma; HeLa, cervical carcinoma; THP-1, acute myeloid leukemia (M5); CCRF-CEM, T-cell acute lymphoblastic leukemia; HEL, acute myeloid leukemia (M6); Raji, Burkitt‘s lymphoma; CTV-2, acute myeloid leukemia (M5); 5637, bladder carcinoma; BT474, breast adenocarcinoma; COLO-206F, colon adenocarcinoma; COLO-680N, esophagus squamous cell carcinoma; A498, renal carcinoma; HEP-3B, hepatocellular carcinoma; A-549, lung adenocarcinoma; COLO-800, melanoma; SK-N-MC, neuroblastoma; MHH-ES-1, Ewing’s sarcoma; COLO-704, ovarian adenocarcinoma. Ten micrograms of total RNA isolated from the indicated cell lines, MA-T1A1 tumor cells (lane 9 in A) and NIH/3T3 cells (lane 10 in A), was submitted to Northern transfer. (A) Filters were hybridized simultaneously with a³²P-labeled myeov cDNA insert and a murine glyceraldehyde 3-phosphate dehydrogenase (GAPDH) probe. Bothmyeov transcripts of 2.8 and 3.5 kb and the GAPDH transcript are indicated at the left side. Almost equal amounts of RNA were loaded in each lane as indicated by the GAPDH hybridization. The stronger hybridization of the 2 murine RNAs (MA-T1A1 and NIH/3T3, lanes 9 and 10) can be explained by the weaker hybridization of the murine GAPDH probe to the human homolog. (B) Filters were hybridized with the samemyeov cDNA insert; 28S and 18S ribosomal RNA were used as molecular weight markers. The lower panel shows the ethidium bromide-stained gel as a control for the amount of RNA loaded in each lane.