TABLE 6.
Tumor type | Drug resistance | Mechanisms | References |
ALL | ASNase | CAAs producing both ASN and GLN, counteracting the effects of ASNase. | Ehsanipour et al., 2013 |
Vincristine | CAAs secreting SDF-1α, promoting the migration of ALL toward adipose tissue. | Pramanik et al., 2013 | |
Daunorubicin | CAAs decreasing daunorubicin concentration in ALL cells by expressing daunorubicin-metabolizing enzymes. | Sheng et al., 2017 | |
Breast cancer | Trastuzumab | Adipose-derived factors decreasing the secretion of INF-γ in natural killer cells. | Duong et al., 2015 |
Doxorubicin | CAAs inducing the overexpression of MVP in tumor cells, increasing drug efflux and decreasing drug intracellular accumulation. | Lehuédé et al., 2019 | |
CRC | 5-FU | CAAs secreting leptin activating the PI3K/AKT signaling pathway. | Bartucci et al., 2010 |
Myeloma | Bortezomib | CAAs derived leptin promoting the activation of JAK/STAT-PI3K/AKT pathway. | Yu et al., 2016 |
Melphalan, bortezomib | CAAs derived adipokines activating JAK/STAT3 signaling and inducing the upregulation of autophagic proteins, promoting autophagy. | Liu Z. et al., 2015 | |
Ovarian cancer | Paclitaxel | CAAs-derived exosomes transferring higher levels of miR21 to the cancer cells. | Yeung et al., 2016 |
Cisplatin | CAAs releasing AA, activating the Akt pathway in ovarian cancer cells. | Yang et al., 2019 | |
Carboplatin | Adipocytes inducing FABP4 expression. | Mukherjee et al., 2020 |
CAAs, cancer associated adipocytes; ALL, acute lymphoblastic leukemia; ASNase, L-asparaginase; ASN, amino acids asparagine; GLN, glutamine; ADCC, antibody-dependent cellular cytotoxicity; CRC, Colorectal cancer; 5-FU, 5-fluorouracil; miR21, microRNA-21; LDs, lipid droplets; ROS, reactive oxygen species; AA, Arachidonic acid; PDAC, pancreatic ductal adenocarcinoma.