respective control. Methyl Jasmonate Alters the Chemosensitivity of Tumor Cells We also analyzed the effect of MJ on the cytotoxicity of cisplatin and the expression of MDR1. has also been evaluated in combination with various therapeutic drugs with promising outcomes (Cesari et al., 2014; Yousefi et al., 2020). The primary mechanism of the antineoplastic activity of MJ is reported to be associated with its ability to dissociate the mitochondrial membrane-bound hexokinase (HK) from voltage-dependent anion channel (VDAC) (Goldin et al., 2008) with cytotoxic consequences in the susceptible malignant cells (Hong et al., 2016; Zhang et al., 2016). Additionally, MJ up-regulates the generation of ROS (Zhang et al., 2016) and shows inhibitory action on the expression of several key metabolic enzymes involved in the oxidative phosphorylation of tumor cells (Li et al., 2017) and pathways of cell death induction (Cesari et al., 2014; Peng and Zhang, 2017; Wang et al., 2018). However, the mechanism(s) implicated in the antineoplastic activity of MJ exhibits tumor-to-tumor variation (Cesari et al., 2014), necessitating investigation of the antineoplastic mechanisms in a tumor-specific manner. T cell neoplastic disorders are complicated for clinical management (Krok\Schoen et al., 2018) with a very high occurrence and mortality rate (Bellei et al., 2012; Park et al., 2017). However, little is understood concerning the mechanisms underlying such antineoplastic action of MJ against cells of T cell malignancies. Moreover, to date, HK 2 is the only known main target ANX-510 of MJ. Thus, there is an immediate need to identify the other probable targets of the MJ. Further, the effect of MJ on the expression of HIF-1, which is considered as the master regulator of tumor metabolism (Nagao et al., 2019), remains unexplored. Nevertheless, HIF-1 is also an upstream regulator of HK 2 (Pezzuto and Carico, 2018). Additionally, the modulatory effect of MJ on Hsp70, which plays a pivotal role as a regulator of tumor cell survival (Tsuchida et al., 2014) and is downstream to HIF-1 (Pezzuto and Carico, 2018), remains unclear. Further, bioinformatics STRING databases strongly indicate the liaison of HIF-1, HK 2, and Hsp70 in a network of closely linked cooperative molecules involved in regulating tumor rate of metabolism and survival (Szklarczyk et al., 2015). However, a comprehensive investigation of MJs effect on the modulation of HIF-1 accompanied by HK 2 and Hsp70 remains to be investigated. Further, the effect of MJ on numerous critical cellular activities of neoplastic cells, including rate of metabolism, pH homeostasis, chemoresistance, and production of tumor-promoting cytokines, remains mostly unexplored. Hence, these guidelines must be examined in detail before medical applications of MJ against the T cell lymphoma individuals. To address these problems, we used a murine transplantable T cell lymphoma designated as Daltons lymphoma (DL), which has been extensively used to understand the host-tumor relationship (Chandran et al., 2016; Koiri et al., 2017; Yadav et al., 2018) and mechanisms of the antineoplastic action of various chemotherapeutic medicines (Pandey et al., 2019; Gupta et al., 2020). DL originated in the laboratory of ANX-510 Dr Albert J. Dalton at NCI, Bethesda, United States (Goldie and Felix, 1951; Dunham and Stewart, 1953) like a spontaneous thymoma and was later on adapted for ascitic tumor growth (Klein, 1951). The availability of important protein crystals on protein ANX-510 data banks and their utilization for prediction of active sites and molecular docking techniques to product the understanding of the molecular mechanisms underlying drug-target relationships (Li et al., 2020) have given new sizes to the knowledge of the drug-target relationships. Till now, there CDC25A has been no study with this direction using MJ. Hence, it is essential to generate and investigate the molecular docking data of MJ with essential metabolic and cell survival ANX-510 regulatory targets, which have remained entirely.