Arrest of cell growth in the G1 phase of the cell cycle by serine deprivation

Allen, Robert W.; Moskowitz, Merwin

doi:10.1016/0014-4827(78)90070-8

Cited by 27 publications

(20 citation statements)

References 14 publications

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“…Defects in one-carbon metabolism have been implicated in several disease states, including neural tube defects during embryonic development ( 1 ) and cancer ( 2 ). The nonessential amino acid serine is the major source of one-carbon units in proliferating lymphocytes ( 3 , 4 ) and cancer cells ( 5 , 6 ). Serine is broken down into glycine and a one-carbon unit, which can then be incorporated into purines, thymidylate, and methionine.…”

Section: Introductionmentioning

confidence: 99%

Serine one-carbon catabolism with formate overflow

et al. 2016

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Section: Introductionmentioning

confidence: 99%

Serine one-carbon catabolism with formate overflow

et al. 2016

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“…Those causing down-regulation of cell growth and induction of cellular quiescence include high cell density (Stoker, 1972), low serum concentration (Talavera and Basilico, 1978;Yen and Pardee, 1978a;Tupper et al, 19821, nutrient deficiencies (Ross and Sinclair, 1972;Holley and Kiernan, 1974;Yen et al, 1977;Bauer and Dethlefsen, 19811, and a variety of specific chemical deficiencies such as oxygen (in hypoxia) (Harris et al, 1970;Koch et al, 1973;Bedford and Mitchell, 1974;Pallavicini et al, 19791, calcium (Paul and Ristow, 1979;Tupper et al, 1982;Parsons et al, 19831, and amino acids (Allen and Moskowitz, 1978;Talavera and Basilico, 1978;Yen and Pardee, 197813). Almost without exception, induction of quiescence under these circumstances results in the accumulation of cells in the GI phase of the cell cycle.…”

mentioning

confidence: 97%

Cell cycle regulation by environmental pH

Taylor

Hodson

1984

Journal Cellular Physiology

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Purified populations of quiescent human tumour cells were isolated from plateau phase cultures of PMC-22 cells by centrifugal elutriation. Dilution into fresh medium resulted in these quiescent cells entering S phase exponentially with a t1/2 of 12 hr, after a 18-20-hr lag period during which cellular RNA content increased. Subsequent studies showed that recruitment of quiescent cells into the cell cycle could be regulated by extracellular pH. When exponentially growing PMC-22 cells were exposed to acidic extracellular pH levels, three growth patterns were observed: 1) Normal growth between pH 7.2 to pH 6.8; 2) A reduction in growth rate associated with accumulation of cells with a G1 DNA content between pH 6.7 and 6.4 (this was also shown to occur in a number of other tumour cell lines); 3) Non-cell-cycle-phase-specific arrest of growth at pH levels less than 6.3. Further studies with purified quiescent cell populations showed the possible existence of a pH-dependent restriction point in the G1 phase of these tumour cells. The implications of these observations to tumour biology are discussed.

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“…Determination of radioactivity in each sample was performed according to the procedures described by Allen and Moskowitz (Allen and Moskowitz, 1978).…”

Section: Materials and Methods Cell Culture And Culture Mediamentioning

confidence: 99%

Growth stimulation of Rous sarcoma virus‐transformed BHK cells by biotin and serum lipids

Cheng

Moskowitz

1982

Journal Cellular Physiology

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Biotin or a serum lipid extract stimulated proliferation of G1 arrested Rous sarcoma virus-transformed BHK cells in modified Eagle's MEM (BM). The cells could be maintained continuously in BM plus biotin (BMB), but not in BM plus serum lipid extract (BM X L). Avidin inhibited growth stimulation when added to BMB, but did not inhibit growth when added to BM X L. 14C-acetate incorporation into total cellular lipids was stimulated in BMB, but not in BM. Thin-layer chromatography of the labeled cellular lipid extract indicated that relatively large amounts of 14C-acetate were incorporated into phosphatidylserine and little into the other major phospholipids. In the neutral lipids, the largest amount of incorporation was in cholesterol. G1 arrested cells multiplied rapidly in BM supplemented with dialyzed serum (BM X DS), but they did not multiply in BM with delipidized serum (BM X DLS). The addition of biotin or serum lipid extract to BM X DLS stimulated growth. Growth stimulation in BM X DLS by biotin was inhibited by avidin, but avidin had no effect on growth stimulation by serum lipid extract. Biotin stimulated additional multiplication in BM X DS and avidin inhibited this additional growth stimulation. These results suggest that growth stimulation requires lipids supplied by serum lipids or by de novo synthesis stimulated by biotin. In the absence of serum, the stimulation of the synthesis of growth factor(s) by biotin are also required for continuous multiplication.

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Arrest of cell growth in the G1 phase of the cell cycle by serine deprivation

Cited by 27 publications

References 14 publications

Serine one-carbon catabolism with formate overflow

Serine one-carbon catabolism with formate overflow

Cell cycle regulation by environmental pH

Growth stimulation of Rous sarcoma virus‐transformed BHK cells by biotin and serum lipids

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