Long non-coding RNAs (lncRNAs) have been reported to be crucial modulators in various heart diseases, including myocardial infarction (MI). LncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) has been reported to be highly expressed in MI samples. However, the mechanism and biological function of MALAT1 in myocardial infarction are still marked. Similarly, programmed cell death 4 (PDCD4) was also upregulated in MI samples. Therefore, MALAT1 and PDCD4 were chosen to do further study. At first, qRT-PCR was applied to examine the expression patterns of MALAT1 and PDCD4. The results showed that both MALAT1 and PDCD4 were upregulated in MI mice model and the hypoxia-induced myocardial cell. Subsequently, loss-of function assays were conducted to examine the impacts of MALAT1 or PDCD4 on cellular processes. Results of MTT assay and flow cytometry analyses manifested that knockdown of MALAT1 or PDCD4 enhanced cell viability, promoted cell cycle progress and suppressed cell apoptosis. Transferase-mediated dUTP nick end labeling (TUNEL) assay revealed that MALAT1 knockdown or PDCD4 knockdown decreased cell apoptosis in MI mice model. Subsequently, mechanism experiments revealed that microRNA-200a-3p (miR-200a-3p) could bind to either MALATA1 or PDCD4. Combining with the cytoplasmic location of MALAT1, we confirmed that MALAT1 acted as a competing endogenous RNA (ceRNA) to upregulate PDCD4 by sponging miR-200a-3p. Finally, rescue assay suggested that MALAT1-miR-200a-3p-PDCD4 axis regulated the proliferation, cell cycle progression and apoptosis of hypoxia-induced myocardial cells.