Indoleacetic acid (IAA) is one of the main plant hormones, and regulates plant cell division. We report here the presence and distribution of IAA in human cancer tissues, animal cells and serum, and also the promotive effect of IAA on animal cell division, using parachlorophenoxy-iso-butyric acid (PCIB) as an IAA antagonist. Finally, we report some survey on fluctuation of urine and serum IAA before and after resection of human cancer. Acidic substances in the ethanolic extracts of the tissue or cells were paper chromatographed and the parts of the chromatograms having the same
Rfs as those in the cochromatographed IAA were extracted again in ether. IAA in the ether extracts was identified by gas chromatography and/or gas-mass spectrometry. The amount of IAA in the final extracts was bio-assayed by
Avena curvature test or mass fragmentography. In cases of human gastric, esophagus, jejunum, colon, rectum and mammary cancers, IAA content in resected tissues was highest in cancerous regions, next in surrounding areas of cancer and lowest in normal areas. In advanced cases, it was highest in the surrounding areas of cancer and low in cancerous regions. IAA is distributed not only in plant but also in all the animal materials being examined here. So we tried to find the role of IAA in animal cell division and cancer growth. First and 2nd division of sea urchin eggs were accelerated by IAA, and retardeation of embryo development by PCIB was neutralized by IAA. Growth rate of cultured mouse cells, LP-3, in a synthetic medium seemed to be proportional to the amount of bio-synthesized IAA. Another cultured mouse cells, 3T3, and chick embryo heart fibroblasts needed FCS for their growth, but they could also synthesize IAA. Their growth rates in the IAA-free medium seemed to depend on the
de novo synthesized IAA. And the cell division of, chick embryo heart fibroblast cells was also accelerated by exogenously applied IAA and retarded by PCIB, however, this retardation was cancelled by the addition of IAA. These experimental results seem to support the assumption that IAA is one of the regulating factors of animal cell division, and of cancer cell multiplication. The increased amount of urinary and serum IAA in cancer patients decreased after curative resection and became normal in half a month to ten months after surgery.
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