In normal tissue
A study of the ABCC10 promoter revealed that the presence of E2F and Sp1 sites are required for maximum transcription. In addition other elements were found in the promoter including: cAMP-responsive element binding protein, estrogen receptor binding site, hepatic nuclear factor, progesterone receptor binding site, and sterol regulatory element binding protein (Dabrowska and Sirotnak, 2004).
ABCC10 transcript is widespread at low levels (Hopper et al., 2001; Maher et al., 2005) with highest expression in the pancreas. Decreased expression is observed in activated resting T and B cells (Takayanagi et al., 2004).

In cancer
In cell lines: In terms of cancer, the ABCC10 gene is expressed in human tumor cell lines, HepG2, CWR22RV1 and TSU-PR1 at greater or equal levels than ABCC1, ABCC2 and ABCC3. Novel ABCC10 transcripts have been identified in HepG2, and CWR22RV1 cells. These transcripts are heterogeneic and imply complexity in the exons and introns of this region (Dabrowska and Sirotnak, 2004).
In breast cancer: ABCC10 transcript is upregulated in breast tumors treated with 5-fluorouracil, anthracycline, cyclophosphamide or taxane based neoadjuvant chemotherapy in comparison with normal tissue. Further, ABCC10 transcript expression is associated with ER positive breast cancer (Hlavac et al., 2013).
In acute myeloid leukemia: ABCC10 transcript is also expressed in acute myeloid leukemia (Hu et al., 2011).
In hepatocellular carcinoma: Transcripts from ABCC10 and various other transporters including: ABCB6, ABCC1, ABCC4, ABCC5, and ABCC12 are upregulated in over 50% hepatocellular carcinoma in untreated patients. It was also observed that microRNA let-7a/e is able to downregulate ABCC10 transcript (Borel et al., 2012).

In vivo
Abcc10 protects thymus, spleen and bone marrow when exposed to paclitaxel in vivo. Abcc10 loss promotes loss of white blood cells, increased weight loss and increased lethality in mice exposed to high doses of paclitaxel (Hopper-Borge et al., 2011).