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Findings suggest that ANT2 overexpression contributes to EGFR-TKI resistance in non-small cell lung cancer.
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Study found that ANT2 was upregulated in sorafenibresistant hepatocellular carcinoma Huh7 cell line and its overexpression promoted sorafenib resistance.
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cancer cells require both hANT2 and hANT3, depending on their proliferation status: hANT2 when proliferation rates are high, and hANT3 when proliferation slows.
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ANT2 shRNA downregulates miR-19a and miR-96 through the PI3K/Akt pathway and suppresses tumor growth in hepatocellular carcinoma cells.
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IFNgamma induces oxidative stress, DNA damage and tumor cell senescence via TGFbeta/SMAD signaling-dependent induction of Nox4 and suppression of ANT2
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TGF-beta-mediated suppression of ANT2 through NF1/Smad4 complexes contributes to oxidative stress and DNA damage during induction of cellular senescence.
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Sirt4 regulates ATP levels via ANT2 and a feedback loop involving AMPK.
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ANT2 suppression by shRNA may be able to exert anticancer effects in HCC further by restoring SOCS1 expression
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SLC25A5 is involved in memory formation or establishment, which could add mitochondrial processes to the wide array of pathways that regulate normal cognitive functions.
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miR-636 might function as a tumor suppressor miRNA affecting hepatocellular carcinoma (HCC) tumorigenesis via downregulation of Ras, and that ANT2 suppression by shRNA could exert an anticancer effect by restoring miR-636 expression in HCC.
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Apigenin upregulates DR5 and enhances TRAIL induced apoptosis by binding and inhibiting ANT2.
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Compares and contrasts all the known human SLC25A* genes and includes functional information.
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The mammalian proteins MMS19, MIP18, and ANT2 are involved in cytoplasmic iron-sulfur cluster protein assembly.
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In the context of ovarian cancer, the interaction between CKIepsilon and ANT2 mediates pathogenic signalling that is distinct from the canonical Wnt/beta-catenin pathway and is essential for cell proliferation and is clinically associated with poor survival.
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ANT2 is not pro-apoptotic and may therefore contribute to carcinogenesis.
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ANT2 shRNA treatment sensitized MCF7, T47 D, and BT474 cells to TRAIL-induced apoptosis by up-regulating the expression of TRAIL death receptors 4 and 5 (DR4 and DR5) and down-regulating the TRAIL decoy receptor 2 (DcR2).
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ANT2 is able to restore growth on a nonfermentable carbon source of a yeast mutant strain lacking its three endogenous ANC.
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enhanced binding of NF1 is a key step in the growth arrest repression of ANT2 transcription.
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expression under hypoxic conditions alters cell cycle in cancer cells
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Growth-dependent repression of human adenine nucleotide translocator-2 (ANT2) transcription.
