Conclusions
By regulating MALAT1 and NKILA, we controlled the growth and apoptosis of Rb cells, which was expected to be a potential clinical therapeutic target for Rb.
Methods
Tixty-eight cases of retinoblastoma patients admitted to our hospital from February 2017 to February 2019 were collected as a research group, while 70 healthy people who came to our hospital for checkup at the same time were chosen as a control group. Both retinoblastoma and human colorectal mucosa cells were purchased, expression and clinical value of NKILA and MALAT1 in serum of Rb patients were tested, and sh-NKILA, si-NKILA, NC, sh-MALAT1 and si-MALAT1 were transfected into Weri-Rb1 and Y79 cells. qRT-PCR was adopted to detect the NKILA and MALAT1 levels in samples, and WB was adopted to detect the cle-caspase-3, cle-caspase-9, Bax, Cyclin B1, CDC2 and p-CDC2 protein levels in cells. Cell proliferation was conducted via MTT assay, invasion was carried out through transwell assay, and apoptosis was confirmed by flow cytometry assay.
Objective
To assess the expression of LncRNA NKILA and MALAT1 in retinoblastoma and its related mechanisms. Patients and
Results
NKILA and MALAT1 were low expressed in retinoblastoma, and AUC of LncRNA NKILA and MALAT1 was over 0.8. LncRNA NKILA and MALAT1 were associated with tumor size, classification and clinical grading in children with retinoblastoma. Over-expression of NKILA and MALAT1 could promote apoptosis, inhibit cell growth and Bcl-2 protein, and promote upregulation of the expression levels of clecaspase-3, clecaspase-9 and Bax. Conclusions: By regulating MALAT1 and NKILA, we controlled the growth and apoptosis of Rb cells, which was expected to be a potential clinical therapeutic target for Rb.