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Table 1 Overview of HIF-1-mediated mechanisms in drug resistance

From: Role of hypoxia in cancer therapy by regulating the tumor microenvironment

Resistance phenotypeCancer/Cell typeResistant chemotherapy drugMolecular basisReference
Overexpression of drug efflux proteinsColon cancer cells5-FluorouracilMDR1/P-gp[26]
Overexpression of drug efflux proteinsOvarian carcinoma cellsEstramustineABCA2[27]
Overexpression of drug efflux proteinsLung adenocarcinoma cellsAdriamycinP-gp[28]
Apoptosis inhibitionBreast cancer cellsPaclitaxelCaspases 3, 8, 10, and Bak[29]
Apoptosis inhibitionColon cancer cellsEtoposide and oxaliplatinBid and Bax[30]
Apoptosis inhibitionGastric cancer cells5-Fluorouracil and cisplatinp53 and NF-kB[31]
Apoptosis inhibitionHuman melanoma cellsNot mentionedP53 and TRP2[88]
Autophagy inductionHeLa cellsN-(4-Hydroxypheny) retinamide (4-HPR)Beclin1[32]
Autophagy inductionGastric cancer cellsVincristinemiR-23b-3p, ATG12, and HMGB2[33]
Autophagy inductionColon cancer cellsCryptotanshinone Dihydrotanshinonep53[34]
DNA damage inhibitionMouse embryonic fibroblastsEtoposideDNA–PKcs and Ku80[35]
DNA damage inhibitionBreast and liver cancer cellsTaxol and etoposideTMEM45A[36]
Mitochondrial activityHuman leukemia cell line (HL-60) human lymphoma cell line (Raji)Doxorubicin and ara-cBAD[37]
Mitochondrial activityRenal carcinoma cellsNot mentionedVHL[38]
Mitochondrial activityOral squamous cell carcinoma cells5-Fluorouracil and cisplatinCytochrome, Akt, and ERK[39]
P53Non-small-cell lung cancer cellsCisplatinHIF-1α and BAX[40]