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Antigenic Phenotype and Biological Characteristics of Two Distinct Sublines Derived from a Small Cell Lung Carcinoma Cell Line¹

Laboratories of Chemotherapy [H. W., R. U.,], Cell Biology [K. R. U.], and Immunology [To. T., Y. O.], Internal Medicine [Y. A., K. O.], and Clinical Laboratory [T. S.], Aichi Cancer Center, Chikusa-ku, Nagoya 464 and Department of Thoracic Surgery [Ta. T.], Nagoya University School of Medicine, Showaku, Nagoya 466, Japan

Two sublines, SCLC-MOA1 (MOA1) and SCLC-MOA2 (MOA2), were established from the SCLC-MO cell line, which was originally derived from an oat cell type of small cell lung carcinoma (SCLC). SCLC-MO showed typical culture morphology of SCLC, growing as tightly packed floating aggregates, while both MOA1 and MOA2 grew as a monolayer. MOA2 showed markedly shorter culture doubling time and higher colony forming efficiency than SCLC-MO and MOA1. When transplanted into nude mice, both SCLC-MO and MOA1 showed intermediate cell type histology, while MOA2 showed a picture of large cell carcinoma as non-SCLC. As for biomarkers, SCLC-MO showed a transitional state between the classic and the variant types, while MOA1 was the variant type. In contrast, MOA2 lost the biomarker characteristic of SCLC, showing rather non-SCLC type.

SCLC-MO expressed NE-150 neuroendocrine antigen, but lacked PE-35 panepithelial antigen which is generally present on SCLC. It lacked also OE-130 epithelial antigen which is generally absent from SCLC. Thus, the phenotype was NE-150⁺/PE-35^-/OE-130^-, which was different from the major phenotype of SCLC, NE-150⁺/PE-35⁺/OE-130^-. MOA1 was weakly positive for PE-35, showing NE-150⁺/PE-35^±/OE-130^-, while MOA2 was positive for OE-130, but lost NE-150, i.e., NE-150^-/PE-35⁺/OE-130⁺, showing a non-SCLC phenotype. Thus, a good concordance was observed between the antigenic phenotype and the biological characteristics of these SCLC lines. The results altogether suggested that a part of large cell carcinoma in the tumor of the patient may be derived from SCLC.

Karyotype analysis showed that there were several marker chromosomes including deletion of chromosome 3p shared by these three cell lines, supporting the belief that MOA1 and MOA2 originated from SCLC-MO. Southern blot analysis showed the amplification of the L-myc related gene, probably rearranged L-myc, in the primary SCLC tumor as well as in SCLC-MO and MOA1. Northern blot analysis showed the 2.2-kilobase transcripts hybridized with a L-myc probe were observed in SCLC-MO and MOA1, but not in MOA2. In contrast, the c-myc transcript was detected only in MOA2. The activity of the myc gene family may contribute to certain biological characteristics of SCLC.

¹ This work was supported in part by a Grant-in-Aid for the Comprehensive Ten-Year Strategy for Cancer Control from the Ministry of Health and Welfare; Grants-in-Aid for Cancer Research from the Ministries of Education, Science, and Culture and of Health and Welfare in Japan; and by grants from the Cancer Research Institute, Inc., New York, NY, and from the Foundation for Promotion of Cancer Research, Tokyo, Japan.

² To whom requests for reprints should be addressed.

Received 9/ 8/87. Revised 1/11/88. Accepted 2/ 1/88.