Objective To investigate the effect of KHSRP on the malignant biological behavior of lung adenocarcinoma by targeting JAK1/STAT3 signaling axis. Methods The clinical data of 64 cases of LUAD tissues and adjacent tissues diagnosed in Huaihe Hospital from January 2017 to December 2018 were collected. The expression level of KHSRP in LUAD tissues and adjacent tissues was observed by immunohistochemical staining. qRT-PCR was used to detect the expression of KHSRP in lung adenocarcinoma cell lines (SPC-A1, H1975, CL1-5, PC-9, Calu-3, H446) and normal human bronchial epithelial cell line (NHBE). Lentivirus transfection changed the expression of KHSRP in lung adenocarcinoma cell lines SPC-A1, H1975, PC-9 and Calu-3. Cell counting kit-8 (CCK-8) and Transwell assay were used to determine the effect of KHSRP on the proliferation, migration and invasion of lung adenocarcinoma cells. Detection to knock down and xenograft tumor model expression KHSRP in living animals. WB experiment KHSRP targeted JAK/STAT signaling pathway. Rescue experiment was conducted to verify whether KHSRP promotes malignant progression of LUAD cells by regulating JAK1/STAT3 signaling pathway. Results Compared with adjacent normal tissues, KHSRP expression in LUAD organizations significantly higher (P<0.05). Overexpression of KHSRP significantly promoted the proliferation, migration and invasion of LUAD cells in vitro (P<0.05). The results of in vivo animal experiments showed that KHSRP can promote LUAD cell xenograft tumor growth and lung nodule metastasis in nude mice (P<0.01). After KHSRP knockdown, the levels of JAK1, p-JAK1 and STAT3 in JAK/STAT signaling pathway were significantly decreased, while the situation was opposite after KHSRP overexpression (P<0.05). Rescue experiment showed that KHSRP can reverse the inhibitory effect of knockdown (P<0.05). Conclusion KHSRP targets JAK1/STAT3 signaling pathway and acts as an oncogene in lung adenocarcinoma.