beta-elemene　has　a　variety　of　anti-inflammatory,　antioxidant,　and　antitumor　effects.　Currently,　the　influence　of　beta-elemene　on　adrenocortical　carcinoma　(ACC)　malignant　progression　and　action　mechanism　remains　unclear.　This　research　aims　to　explore　the　influence　and　action　mechanism　of　beta-elemene　on　ACC　progression.　The　impacts　of　beta-elemene　on　ACC　cell　viability,　proliferation,　migration,　and　apoptosis　were　investigated　through　CCK-8　assay,　clone　formation　assay,　Transwell　experiment,　Wound　healing　assay,　and　flow　cytometry.　The　miR-486-3p　expression　was　analyzed　utilizing　RT-qPCR.　According　to　different　databases,　neuronal　pentraxin　1　(NPTX1)　is　the　predicted　downstream　target　gene　of　miR-486-3p.　Western　blot　and　RT-qPCR　were　utilized　to　examine　NPTX1　expression.　Silencing　miR-486-3p　or　Overexpression　NPTX1　in　ACC　cells　further　explored　whether　beta-elemene　affects　ACC　cells　by　regulating　miR-486-3p/NPTX1.　Finally,　a　subcutaneous　graft　tumor　model　was　constructed　to　investigate　how　beta-elemene　may　impact　tumor　growth　in　vivo.　beta-elemene　decreased　the　cell　viability,　hindered　cell　proliferation　and　migration　capacity,　and　induced　apoptosis　of　ACC　cells.　miR-486-3p　level　in　ACC　cells　was　notably　reduced　in　comparison　to　normal　cells,　but　treatment　with　beta-elemene　markedly　increased　miR-486-3p　expression.　Additionally,　ACC　cells　showed　high　level　of　NPTX1,　while　miR-486-3p　targeted　negative　regulation　of　NPTX1.　Overexpression　miR-486-3p　hindered　the　malignant　progression　of　ACC　cells,　whereas　overexpression　NPTX1　reversed　the　impact　of　overexpression　miR-486-3p.　Silencing　miR-486-3p　or　overexpression　NPTX1　both　attenuated　the　suppressive　influence　of　beta-elemene　on　the　malignant　behavior　of　ACC　cells.　Additionally,　tumor　growth　was　suppressed　and　apoptosis　was　induced　in　tumor　cells　in　vivo　by　beta-elemene.　In　conclusion,　beta-elemene　reduces　ACC　cell　viability,　hinders　proliferation　and　migration,　and　induces　apoptosis　through　the　miR-486-3p/NPTX1　axis.