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The natural protein kinase C alpha mutant is present in human thyroid neoplasms.
Oncogene. 1995 Aug 17; 11(4):669-74.O

Abstract

An altered protein expression of Ca(2+)-dependent protein kinase C (PKC) isoforms and a point mutation in the PKC alpha cDNA (position 908 of the nucleotide sequence, position 294 of the amino acid sequence, substitution of an aspartic acid by a glycine) have been previously described in a subpopulation of human pituitary tumors. In this work, we screened 16 thyroid tissue samples (four follicular adenomas, five colloid adenomas, three papillary carcinomas, one follicular carcinoma and three normal tissues adjacent to the tumors) for the presence of the PKC alpha point mutation and for PKC alpha, beta 1, beta 2, epsilon and delta protein expression. Screening for the presence of the PKC alpha mutant was performed by a subcloning technic. The polymerase chain reaction products were generated using reverse-transcribed cDNAs, subcloned and sequenced (10 clones were routinely sequenced). The PKC alpha point mutation at position 908 of the cDNA sequence was found in four out of the nine adenomas and in the follicular carcinoma. It was neither detected in the papillary carcinomas nor in the adjacent normal tissues (one was the adjacent normal tissue of the follicular carcinoma; in this sample, genomic DNA and cDNA were used to look for the presence of the mutant), demonstrating the somatic nature of this mutant. Western blot analysis of PKC isoforms showed that the expression of all isoforms was higher in the thyroid neoplasms as compared with their adjacent normal tissue (n = 3). It was also higher in the samples containing the PKC mutant (two follicular adenomas, two colloid adenomas and the follicular carcinoma) as compared with the tumors where it was not detected (three papillary carcinomas and five adenomas). Samples could be ordered according to their increasing PKC expression as follows: normal adjacent tissue < follicular adenomas without PKC alpha mutant < or = papillary carcinoma < follicular adenomas with PKC mutant < follicular carcinoma with PKC mutant. In conclusion, the discovery of the PKC alpha mutant in thyroid neoplasms demonstrates that this mutant is not particular to human pituitary tumors where it was originally detected. It is a somatic mutation and its presence is concomitant with high levels of all of the PKC isoforms analysed. The presence of the PKC mutant in thyroid neoplasms raises the question of its importance in thyroid tumorigenesis.

Authors+Show Affiliations

INSERM U401, Montpellier, France.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

7651730

Citation

Prévostel, C, et al. "The Natural Protein Kinase C Alpha Mutant Is Present in Human Thyroid Neoplasms." Oncogene, vol. 11, no. 4, 1995, pp. 669-74.
Prévostel C, Alvaro V, de Boisvilliers F, et al. The natural protein kinase C alpha mutant is present in human thyroid neoplasms. Oncogene. 1995;11(4):669-74.
Prévostel, C., Alvaro, V., de Boisvilliers, F., Martin, A., Jaffiol, C., & Joubert, D. (1995). The natural protein kinase C alpha mutant is present in human thyroid neoplasms. Oncogene, 11(4), 669-74.
Prévostel C, et al. The Natural Protein Kinase C Alpha Mutant Is Present in Human Thyroid Neoplasms. Oncogene. 1995 Aug 17;11(4):669-74. PubMed PMID: 7651730.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The natural protein kinase C alpha mutant is present in human thyroid neoplasms. AU - Prévostel,C, AU - Alvaro,V, AU - de Boisvilliers,F, AU - Martin,A, AU - Jaffiol,C, AU - Joubert,D, PY - 1995/8/17/pubmed PY - 1995/8/17/medline PY - 1995/8/17/entrez SP - 669 EP - 74 JF - Oncogene JO - Oncogene VL - 11 IS - 4 N2 - An altered protein expression of Ca(2+)-dependent protein kinase C (PKC) isoforms and a point mutation in the PKC alpha cDNA (position 908 of the nucleotide sequence, position 294 of the amino acid sequence, substitution of an aspartic acid by a glycine) have been previously described in a subpopulation of human pituitary tumors. In this work, we screened 16 thyroid tissue samples (four follicular adenomas, five colloid adenomas, three papillary carcinomas, one follicular carcinoma and three normal tissues adjacent to the tumors) for the presence of the PKC alpha point mutation and for PKC alpha, beta 1, beta 2, epsilon and delta protein expression. Screening for the presence of the PKC alpha mutant was performed by a subcloning technic. The polymerase chain reaction products were generated using reverse-transcribed cDNAs, subcloned and sequenced (10 clones were routinely sequenced). The PKC alpha point mutation at position 908 of the cDNA sequence was found in four out of the nine adenomas and in the follicular carcinoma. It was neither detected in the papillary carcinomas nor in the adjacent normal tissues (one was the adjacent normal tissue of the follicular carcinoma; in this sample, genomic DNA and cDNA were used to look for the presence of the mutant), demonstrating the somatic nature of this mutant. Western blot analysis of PKC isoforms showed that the expression of all isoforms was higher in the thyroid neoplasms as compared with their adjacent normal tissue (n = 3). It was also higher in the samples containing the PKC mutant (two follicular adenomas, two colloid adenomas and the follicular carcinoma) as compared with the tumors where it was not detected (three papillary carcinomas and five adenomas). Samples could be ordered according to their increasing PKC expression as follows: normal adjacent tissue < follicular adenomas without PKC alpha mutant < or = papillary carcinoma < follicular adenomas with PKC mutant < follicular carcinoma with PKC mutant. In conclusion, the discovery of the PKC alpha mutant in thyroid neoplasms demonstrates that this mutant is not particular to human pituitary tumors where it was originally detected. It is a somatic mutation and its presence is concomitant with high levels of all of the PKC isoforms analysed. The presence of the PKC mutant in thyroid neoplasms raises the question of its importance in thyroid tumorigenesis. SN - 0950-9232 UR - https://www.unboundmedicine.com/medline/citation/7651730/The_natural_protein_kinase_C_alpha_mutant_is_present_in_human_thyroid_neoplasms_ L2 - https://medlineplus.gov/thyroidcancer.html DB - PRIME DP - Unbound Medicine ER -