Hematopoietic-substrate-1 associated protein X-1 (HAX-1) regulates liver cancer cells growth, metastasis, and angiogenesis through Akt

Abstract

The aim of this study was to investigate the effects and mechanisms of hematopoietic-substrate-1-associated protein X-1 (HAX-1) on liver cancer cells. Information on HAX-1 from liver cancer patients was analyzed by the Cancer Genome Atlas (TCGA) program. Cell migration and invasion abilities were respectively tested by scratch assay and transwell assay. Tube formation assay was applied to detect angiogenesis protein and mRNA was determined using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. We found that the median month survival of HAX-1 overexpressing liver cancer patients was shorter than that of HAX-1 normal liver cancer patients. HAX-1 was overexpressed in liver cancer tissues and cells, and HAX-1 overexpression promoted the liver cancer cells growth, migration, and invasion, whereas silencing HAX-1 produced the opposite results. Inhibition of Akt by LY294002 reversed the migration and invasion abilities of liver cancer cells, and inhibited the ability of cells growth and angiogenesis. Silencing PIK3CA enhanced the inhibitory effects of HAX-1 silencing on the viability, migration, and invasion of liver cancer cells. HAX-1 affected liver cancer cells metastasis and angiogenesis by affecting Akt phosphorylation and FOXO3A expression.

MicroRNA‑125a‑5p regulates liver cancer cell growth, migration and invasion and EMT by targeting HAX1

“…Tumor metastasis will result in less desired treatment outcomes of patients with liver cancer (37). The present data suggested that upregulated HAX1 expression promoted the growth, migration and invasion of liver cancer cells, whereas HAX1 knockdown produced the opposite effects, which were in accordance with the results of previous studies (17,34). The present data further confirmed that HAX1 is a tumor oncogene of liver cancer development and might be an underlying target for the treatment of liver cancer.…”

“…HAX1 is a prognostic factor and is abnormally expressed in several types of cancer ( 31 - 33 ). Similar to previous results ( 34 ), the present data suggested that high HAX1 expression was associated with poorer prognosis in the liver cancer tissues and cell lines examined. The data demonstrated that HAX1 might be an oncogene for liver cancer progression and have diagnostic and prognostic values for liver cancer.…”

QPCT regulation by CTCF leads to sunitinib resistance in renal cell carcinoma by promoting angiogenesis

“…7B). These results were consistent with those of certain previous studies suggesting that PIK3CA overexpression promotes angiogenesis (19)(20)(21)(22).…”

“…PIK3CA was involved in the PI3K/AKT pathway, which plays a crucial biological role in cell growth, proliferation, apoptosis, angiogenesis, autophagy and other cell processes. The disruption of this pathway leads to a range of diseases, including cancer (19)(20)(21). The present study verified the results of ChIP with co-IP, and PIK3CA was proven capable of combining with QPCT (Fig.…”

“…The disruption of this pathway leads to a range of diseases, including cancer (44). PI3K/Akt/mTOR pathway plays an important role in the regulation of angiogenesis in normal and cancerous tissues (19)(20)(21)(22)39). PI3K proteins are a family of lipid kinases that are activated in growth factor receptor tyrosine kinases (RTKs) and G-protein coupled receptor signaling.…”