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Ethephon is plant growth regulator widely used to control maize lodging at the early stage of jointing. However, the function and efficacy of ethephon due to differences of cultivars and maize growing areas remains elusive, necessitating the evaluation of each cultivar's sensitivities prior to the application of ethylene. In this study, we collected ten maize cultivars from the largest planted area in China and cultivated in three typical growing areas to evaluate their sensitivity to ethephon. The results showed that ethephon reduced maize plant height, ear height, length of base internode, and generally increased the crushing strength of maize base internode. These traits may enhance maize lodging resistance by reducing the center of gravity of the plant structure. The effect of ethephon varied across growing areas, and cultivars within the same region exhibited distinct sensitivity levels to ethephon. The crushing strength of the eighth internode in maize exhibits a wide range of change and small coefficient of variation. Hence, this index's change range could be utilized to assess the sensitivity of maize cultivars to ethephon in various regions. In addition to agronomic traits, we detected shifts in transcriptional levels related to the signaling pathways of phytohormones, particularly ethylene and gibberellin. These changes reveal the association between transcriptional signaling levels of key factors and the sensitivity to ethylene in ten maize cultivars. The results contribute to our understanding of the lodging resistance in different maize cultivars and evaluation the sensitivity of maize cultivar to ethephon in different growing areas, with implications for comparable pedo-climatic conditions elsewhere. [Display omitted] • The sensitivity of same cultivar to ETH differed in different growing areas, and within the same growing area. • The sensitivity of different cultivars to ETH can be evaluated by the crushing strength of maize eighth internode. • The sensitivity of different cultivars to ETH correlated to the expression level of ETH receptor. [ABSTRACT FROM AUTHOR]