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P021

Peptide 021, GLXC-21260

Quick Stats
Studies 37
Trials 57
Score 1
1992 pubmed

Increased growth of NIH/3T3 cells by transfection with human p120 complementary DNA and inhibition by a p120 antisense construct.

Perlaky. L L; Valdez. B C BC; Busch. R K RK; Larson. R G RG; Jhiang. S M SM; Zhang. W W WW; Brattain. M M; Busch. H H

Key Findings

  • Overexpressing human p120 in NIH/3T3 cells caused malignant transformation and rapid tumor growth in mice.
  • Introducing antisense p021 reduced p120 levels and slowed tumor growth both in vitro and in vivo.
  • Inducing antisense p021 in already transformed cells restored a normal phenotype and cut growth rate by about 62%.

Practical Outcomes

  • For most biohackers, this study offers limited direct use because it involves gene manipulation in lab mice, not a supplement or lifestyle change. It does suggest that targeting p120 could be a strategy to control unwanted cell proliferation, but no safe, real‑world protocol or dosage is provided.

Summary

Scientists put a human protein called p120 into mouse cells and saw the cells turn cancer‑like and grow fast. When they added a matching antisense piece (p021) that blocks p120, the cells grew slower and looked normal again. This shows p120 can drive cell growth, and blocking it can reverse that effect, but the work was done in cell cultures and mice, not people.

Abstract

The human nucleolar antigen p120 was detected with an anti-p120 monoclonal antibody in most human malignant tumors but not in most resting human tissues (J. W. Freeman et al., Cancer Res., 48: 1244-1251, 1988) and has been used as a prognostic tumor marker in breast cancer patients (J. W. Freeman et al., Cancer Res., 51: 1973-1978, 1991). After the complementary DNA and gene for the human p120 protein were isolated and sequenced (review: H. Busch, Cancer Res., 50: 4830-4838, 1990), constructs were prepared to study the expression of the sense p120 and its antisense, p021 message. NIH/3T3 cells were transfected by electroporation with pSVX plasmids containing either the p120 complementary DNA (pSVX120) or the antisense, p021 DNA (pSVX021), and clones containing these constructs were selected. The expression of p120 or p021 in these constructs was regulated by Moloney murine leukemia virus long terminal repeats. In pSVX120-transfected NIH/3T3 cells, the expressed human p120 protein was localized to the nucleoli as shown by anti-p120 monoclonal antibody immunofluorescence. Expression of the p120 message and protein was confirmed by Northern (mRNA) and Western (protein) blots. Transfection of the p120 complementary DNA in sense orientation caused malignant transformation of NIH/3T3 cells in vitro and produced rapidly growing tumors in nude mice. Transfection of the antisense p120 constructs markedly delayed the growth of these tumors in vitro and in vivo (L. Perlaky et al., Proc. Am. Assoc. Cancer Res., 32: 1682, 1991). When transformed 3T3/pSVX120 cells were transfected with an inducible antisense p120 construct (pMSG021), dexamethasone induction decreased the growth rate by 62%, and the cell line returned to its normal phenotype. Northern blot analysis showed a decreased level of p120 mRNA, and the immunofluorescence was also markedly reduced.

Study Information

Provider

pubmed

Year

1992

Date

1992-01-15T00:00:00.000Z