Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0038187 (
starvation
)
24,951
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The
bystin-like
(
BYSL
) gene was previously characterized to encode an accessory protein for cell adhesion that participates in early embryo implantation. It is also involved in 40S ribosomal subunit biogenesis and is found to be expressed in rapidly growing embryo and cancer cell lines. In order to explore the role of
BYSL
in cancer cell proliferation and growth, we used hepatocellular carcinoma (HCC) as a model. Here, we report that
BYSL
is crucial for HCC cell growth both in vitro and in vivo. Expression levels of
BYSL
mRNA and protein in human HCC specimens were markedly increased compared with those seen in adjacent non-cancerous tissue. In vitro, inhibition of
BYSL
by short hairpin RNA decreased HCC cell proliferation, induced apoptosis and partially arrested the cell cycle in the G2/M phase. In vivo, HCC cells treated with
BYSL
siRNA failed to form tumors in nude mice after subcutaneous implantation. To determine the cellular basis for
BYSL
RNAi-induced cell growth arrest,
BYSL
subcellular localization in mitotic and interphase HepG2 cells was examined.
BYSL
was present at multiple stages during nucleologenesis, including in nucleolus-derived foci (NDF), perichromosomal regions and the prenucleolar body (PNB) during mitosis.
BYSL
depletion remarkably suppressed NDF and PNB formation, and disrupted nucleoli assembly after mitosis, resulting in increased apoptosis and reduced tolerance of HCC cells to serum
starvation
. Taken together, our studies indicate that upregulated
BYSL
expression plays a role in hepatocarcinogenesis.
...
PMID:Bystin-like protein is upregulated in hepatocellular carcinoma and required for nucleologenesis in cancer cell proliferation. 1968 2