Since RMRP was found to target microRNA-766-5p (miR-766-5p) in TNBC cells, it enhanced cell viability anddecreased apoptosis by silencing miR-766-5p. Additionally, RMRP has been proven to be highly involved ineither pathological or physiological processes. Therefore, the study aims to determine whether RMRP promotesthe multiplication, migration, and invasion of gastric cancer cells. The study will overexpress RMRP in GC1401gastric cancer cells and measure cell growth by MTT assay, migration by wound healing assay, and Boyden chamberassay. Positive control is another treatment previously shown to increase cancer cell growth and migration, such asIQGAP3, which, beginning with the early stages of tumor growth, is markedly up-regulated in human stomach cancer.Furthermore, the negative control is DMSO. The study measures miR206 by qRTPCR. If the solution gets dark throughMTT assay, RMRP promotes gastric cancer cell multiplication. If the migration rate is getting quicker according to thewound healing assay, and the number of migration cells increases by Boyden chamber assay, RMRP promotes gastriccancer cell migration. If miR-206 may affect the expression of HIF-1 to control cell growth and ECM buildup, RMRPpromotes gastric cancer cell invasion by acting as a miR-206 sponge for gastric cancer. The RNA component of miRNAprocessing endoribonuclease, the novel biomarker for gastric cancer, promotes gastric cancer cell multiplication,migration, and invasion by acting as a miR-206 loss of function in cell lines for gastric cancer.