Pyridoxal supplementation reduces cell proliferation and DNA synthesis in estrogen-dependent and -independent mammary carcinoma cell lines.
In previous studies, decreased growth of tumor cells by vitamin B-6 treatment has been attributed to modulation of steroid hormone action. Therefore, the growth-inhibiting properties of pyridoxal (PL) supplementation were studied in estrogen receptor-positive, MCF-7 and T-47D, and estrogen receptor-negative, BT-20, breast cancer cell lines. Cell counting and [3H]thymidine incorporation into DNA were used to assess growth, and analysis of pS2 expression was used to determine whether PL supplementation affected estrogen action. Treatment with 100 or 300 mM PL resulted in dose-dependent decreases in total cell numbers in the absence (26-85% and 72-98%, respectively) and presence (38-42% and 88-98%, respectively) of estradiol in all cell lines studied compared with control cells cultured without PL supplementation. Similar decreases in DNA synthesis were observed in response to PL supplementation. Incorporation of [3H]thymidine into DNA of cells cultured with 100 or 300 microM PL was decreased by 30-90% and 96-99%, respectively, in the absence and by 32-40% and 82-99%, respectively, in the presence of estradiol. Northern analysis showed that expression of the estrogen-sensitive gene pS2 was not affected by either concentration of PL. These results indicate that PL supplementation regulates breast cancer cell growth in vitro via a mechanism that appears to be steroid independent.
Davis
B A
BA
Human Nutrition, Foods, and Exercise Department, Virginia Polytechnic Institute and State University, Blacksburg 24060, USA. badavis@vt.edu
Cowing
B E
BE
D000970:Antineoplastic Agents / Q000008:administration & dosage / Q000494:pharmacology; D002277:Carcinoma / Q000378:metabolism / Q000473:pathology*; D002455:Cell Division / Q000187:drug effects; D004273:DNA, Neoplasm / Q000096:biosynthesis* / Q000187:drug effects; D019587:Dietary Supplements; D004305:Dose-Response Relationship, Drug; D004958:Estradiol / Q000378:metabolism; D005260:Female; D006801:Humans; D015674:Mammary Neoplasms, Animal / Q000378:metabolism / Q000473:pathology*; D009376:Neoplasms, Hormone-Dependent / Q000378:metabolism / Q000473:pathology*; D014176:Protein Biosynthesis; D011506:Proteins / Q000187:drug effects / Q000235:genetics*; D011730:Pyridoxal / Q000008:administration & dosage* / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D011960:Receptors, Estrogen / Q000378:metabolism; D000071163:Trefoil Factor-1; D014407:Tumor Cells, Cultured; D025521:Tumor Suppressor Proteins
D000970:Antineoplastic Agents; D004273:DNA, Neoplasm; D011506:Proteins; D012333:RNA, Messenger; D011960:Receptors, Estrogen; C051838:TFF1 protein, human; D000071163:Trefoil Factor-1; D025521:Tumor Suppressor Proteins; D011730:Pyridoxal; D004958:Estradiol