NOT MEDICAL ADVICE!

This scientist explains that basketball players might be LIN28 phenotypes.

In mice with a Hmga2 gene knockout, a dwarf phenotype was observed with a 20% reduction in body size in heterozygous mice and a 60% reduction in homozygous mice, in another study - 75%:

Hmga1 −/− /Hmga2 −/− mice showed a decrease in viability and a very small size (75% smaller than wild-type mice)

Pathway: c-Myc -> Lin28 (increase) -> Let-7 (inhibition) -> HMGA2 (increase)

DGAP103" - a 8 year old child is 5'7 (169cm)!!

So far this seems like a very good and promising thing to approach.

BUT there is a big problem.

After birth body undergoes a switch

DNMT's add methyl groups to the promoters of fetal growth genes, including HMGA proteins.

There is a way to inhibit DNMT but it is very dangerous and come with alot of side effects so for safety i won't mention any methods on that part i will let you do your own research and think for yourself.

I will stop yapping and talk only about maybe possible ways to increase HMGA2:

TTP:

"Tristetraprolin (TTP) is a AU-rich element (ARE) binding protein and exhibits suppressive effects on cell growth through down-regulation of ARE-containing oncogenes. let-7 microRNA has emerged as a significant factor in [cell growth] suppression{anything that causes cell growth makes cancer grow faster but it doesn't cause cancer}. Both TTP and let-7 are often repressed in human cancers, thereby promoting oncogenesis by derepressing their target genes. TTP promotes an increase in expression of mature let-7{so we can decrease TTP to decrease Let-7}, which leads to the inhibition of let-7 target gene CDC34 expression and suppresses cell growth. [TTP-mediates] inhibition of Lin28. Lin28 mRNA contains ARE within its 3'-UTR and TTP enhances the decay of Lin28 mRNA through binding to its 3'-UTR. TTP-mediated down-regulation of Lin28 plays a key role in let-7 miRNA biogenesis."

SOX2:

Fig. 1. SOX2 regulates the expression of LIN28. (A) Immunostaining for SOX2 and LIN28 in hESC-derived NPCs. (B) qPCR analysis of SOX2 (Left) and LIN28 (Right) expression following SOX2 knockdown in hESC-derived NPCs. shRNA was induced by dox on day 0. Data are normalized to HPRT. shSOX2, SOX2 shRNA; shCTRL, scrambled shRNA. (C) Western blot for SOX2 and LIN28 in SOX2 knockdown cells 3 d after dox induction. (D) Immunostaining for LIN28 in SOX2 knockdown and control NPCs 3 d after dox induction. (E) qPCR analysis of SOX2 and LIN28 expression in ventralized NPCs 3 d after dox induction. (F) Immunostaining for SOX2 and LIN28 in fetal neural tubes (E11) of wild-type (Sox2+/+) and SOX2 knockout (Sox2flox/flox) mice with conditional deletion in the dorsal neural tube (Wnt1-Cre::Sox2flox). (G) Quantification of LIN28 fluorescence shown in F. (H) Immunostaining for LIN28 in the subgranular layer of the adult hippocampal dentate gyrus in wild-type (Sox2+/+) and SOX2-deleted (Sox2flox/flox) mice. (I) Quantification of LIN28 fluorescence in CFP+ cells shown in H. (J) Immunostaining for LIN28 in the subventricular zone of wild-type (Sox2+/+) and SOX2-deleted (Sox2flox/flox) mice. (K) Quantification of LIN28 fluorescence in CFP+ cells shown in J. **P < 0.005. Nestin-CFPnuc transgene labels neuronal precursors in H and J. Nuclei are in blue (DAPI). (Scale bars: 50 µm.) Error bars ± SE.

Conclusion:

HMGA's are powerfull protein that can drastically increase height/growth

If DNMT is slightly inhibited we can revive HMGA from the silent state

SOX2 is by far the most promising for increasing HMGA2