Protein tyrosyl phosphorylation plays an essential role in regulating
cellular events such as proliferation, differentiation and oncogenesis
. The recent characterization of the family of protein tyrosine phosph
atases (PTPases) suggests that dephosphorylation might be a crucial ev
ent in these phenomena. One of the functions of PTPases is to reverse
the effect of protein tyrosine kinases (PTKases), many of which are on
cogenes, suggesting that they may act as tumor suppressors as describe
d for HPTP gamma. In order to investigate the implication in lung canc
er of HPTP beta, a receptor PTPase, we have developed a semi-quantitat
ive method derived from primer-directed reverse transcription (RT) and
subsequent polymerase chain reaction (PCR) with P-32-labelled nucleot
ide. We have demonstrated that the expression of HPTP beta mRNA was dr
amatically decreased in lung adenocarcinomas and lung malpighian carci
nomas as compared to normal lung tissue. In addition, HPTP beta was no
t expressed in the pulmonar adenocarcinoma cell line A427, which proli
ferates in a deregulated way. These results suggest that the loss of e
xpression of HPTP beta might play a role in neoplasic transformation a
nd thus this molecule could act as a tumor suppressor factor.