<p>The long non-coding RNA Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) is implicated in cancer progression, yet its precise mechanism in nasopharyngeal carcinoma (NPC), particularly its interaction with microRNAs and its role in regulating autophagy, remains to be fully elucidated. We analyzed MALAT1 and miR-28-5p expression in NPC clinical tissues and assessed their correlation with autophagy markers. The direct binding between MALAT1 and miR-28-5p, and between miR-28-5p and Insulin-like Growth Factor 1 Receptor (IGF1R), was validated using dual-luciferase reporter and RNA immunoprecipitation assays. Functional roles in proliferation, apoptosis, migration, and invasion were determined using Cell Counting Kit-8, flow cytometry, Transwell, and wound healing assays. Autophagic activity was evaluated by measuring microtubule-associated protein 1&#xa0;A/1B-light chain 3 (LC3)-II/I ratio and p62 levels and observing autophagosome formation. <i>In vivo</i> tumor growth and autophagy were assessed in a xenograft mouse model. We found MALAT1 was significantly upregulated, and miR-28-5p was downregulated in NPC tissues, showing a significant correlation with autophagic activity. MALAT1 functioned as a competitive endogenous RNA by directly binding to and sequestering miR-28-5p. Subsequently, miR-28-5p was shown to directly target and suppress IGF1R. Overexpression of miR-28-5p curbed NPC cell growth, migration, and invasion and promoted apoptosis, whereas MALAT1 overexpression or IGF1R restoration counteracted these effects. The MALAT1/miR-28-5p/IGF1R axis increased the LC3-II/I ratio, decreased p62, and elevated autophagosome formation. These pro-tumorigenic and pro-autophagic effects were consistently observed <i>in vivo</i>. In conclusion, MALAT1 promotes autophagy by sequestering miR-28-5p to upregulate IGF1R in NPC, providing a novel mechanistic insight and a potential therapeutic target.</p>