[CANCER RESEARCH 58, 4160-4167. September 15. 1998]
Taxol Resistance Mediated by Transfection of the Liver-specific Sister Gene
of P-Glycoprotein1
Sarah Childs, Richard Lin Yeh, David Hui, and Victor Ling2
BC Cancer Research Center. BC Cancer Agencv, University of British Columbia. Vancouver, British Columbia, V5Z IL3 Canada
ABSTRACT
The sister gene of P-glycoprotein (Spgp) is a liver-specific ATP-binding
cassette protein highly related to the P-glycoprotein (Pgp) family (S.
Childs et al, Cancer Res., 55: 2029-2034, 1995). Spgp appears to be
related to the Pgp family by an ancient duplication occurring before the
division of fish and mammals. P-Glycoproteins have diverse functions
including broad specificity multidrug resistance in cell lines and tumors,
detoxification of tissues such as the intestine and blood-brain barrier, and
phosphatidylcholine transport in liver. Spgp is a ,17, —170,000 glycosy-
lated plasma membrane protein localized to the canalicular surface of
hepatocytes in the rat liver. The full-length cDNA of Spgp was isolated
from rat, and its expression was characterized in situ and in transfected
cells. The expression of Spgp correlates with the differentiation of hepa
tocytes and is seen only in late liver development. It is not observed in
hepatoma cell lines. The physiological function of Spgp in liver is un
known, but it maps to 2q31 in humans, in the vicinity of liver transport
disorders for bile acids and cholesterol. Spgp may therefore be involved in
some aspect of bile acid or cholesterol metabolism. Spgp transfectants
have a low level resistance to Taxol but not to other drugs that form part
of the multidrug resistance phenotype. This resistance is reversible by the
Pgp-reversing agents cyclosporin A, PSC833, and verapamil, suggesting a
conservation in some functions of Pgps across large evolutionary distance.
INTRODUCTION
A new member of the P-glycoprotein family of genes called Spgp3
was first identified in pig liver from a partial cDNA sequence (1). It
appears to be a highly liver-specific protein. Its relationship to the Pgp
family is close enough that some nucleic acid probes and antibodies
cross-react with Spgp. However, Spgp is distinct from the Pgp mul-
tigene family and exists as an independent gene in species as distantly
related to mammals as the fish, winter flounder, and minnow (2).4
Thus, the divergence of Spgp and the Pgps probably preceeded the
emergence of the Pgp multigene family (class I, II, and III genes) in
mammalian species. The function of Spgp is unknown, but its evo
lutionary relationship to the P-glycoproteins suggests that it could be
capable of transporting drugs similar to the class I and class II
isoforms, or it could have a basic role in liver physiology similar to the
class III isoform. Although in sequence Spgp does not resemble any
Pgp family member more than any other, its unique liver-specific
expression pattern most closely resembles that of mdr2 encoding the
class III isoform (l).
In liver, the class III isoform of Pgp is a bile canalicular membrane
protein (3). Its physiological function was discovered by analysis of
Received 3/10/98: accepted 7/20/98.
The costs of publication of this article were defrayed in part by the payment of page
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1This work was supported by grants from the National Cancer Institute of Canada (to
V. L.). a National Cancer Institute of Canada Sieve Fonyo Fellowship (to S. C.), and a
Canadian Breast Cancer Foundation Studentship (to D. H.).
2 To whom requests for reprints should be addressed, at BC Cancer Research Centre,
601 West 10th Avenue. Vancouver, British Columbia, V5Z 1L3 Canada. Phone:
(604) 877-6151: Fax: (604) 877-6150; E-mail: vling@bccancer.bc.ca.
3 The abbreviations used are: Spgp. sister gene of P-glycoprotein; Pgp. P-glycoprotein;
PC, phosphatidylcholine; CsA. cyclosporin A: MDR. multidrug resistance: FISH, fluo
rescence in situ hybridization: PAC. PI-derived artificial chromosome; DAPI, 4',6-
diamidino-2-phenylindole; UTR. untranslated region: PFIC2. progressive familial intra-
hepatic cholestasis type 2; cMOAT, canalicular multiple organic anión.
4 P. S. Cooper, personal communication.
mice in which the gene had been "knocked out." These mice exhibited
abnormal liver pathology including proliferation of bile ducts and a
complete absence of PC in bile (4). Subsequent in vitro experiments
have shown that mdr2 encodes a PC translocase, transferring PC from
the inner leaflet of the membrane to the outer leaflet (5). PC, but not
other phospholipids, is an essential component of bile, and by forming
mixed micelles with bile acids, it is thought to prevent the detergent
action of bile from damaging the cells lining the bile ducts.
In contrast, the other members of the Pgp family have been found
to confer broad specificity MDR, transporting a myriad of seemingly
unrelated drugs out of cells using the energy supplied by the hydrol
ysis of ATP (reviewed in Ref. 6). In humans, the overexpression of
MDR 1 has been shown to correlate with poor response to chemother
apy, while coadministering drugs that inhibit Pgp during chemother
apy can improve survival (7, 8).
Studies with mice lacking one or both Pgp genes associated with
MDR have shown that these molecules contribute significantly in
normal physiology to the prevention of drugs crossing the blood-brain
barrier and to the clearance of drugs through the intestine and liver (9,
10). One surprising result from these studies is that Taxol (paclitaxel)
elimination from the liver is normal in the knockout mice, whereas
Taxol elimination from the gut is impaired. This suggested that the
liver has an additional non-Pgp mechanism for transporting Taxol into
bile (10-12). Here we describe the cloning and characterization of
Spgp from rat to gain further insight into its transport specificity and
function to see if it might play a pharmacological role in the elimi
nation of drugs from the liver. At the same time, the specificity of
expression of Spgp in the liver across the entire range of vertebrate
phylogeny suggests that it has a conserved ancient function in the
liver. We have used FISH mapping as a first step to identify putative
physiological functions and substrates.
MATERIALS AND METHODS
Probe Design and cDNA Isolation. The 109-bp GAPIS probe was gen
erated by PCR amplification of the pig spgp sequence5 using the primers
5'-TGCCGTCATGTCACAGGG-3' and 5'-TCAACTGATGGGGGCTCC-3'.
Total RNA was isolated from an adult male Sprague Dawley rat liver by the
cesium chloride density gradient method (13). mRNA was then purified on an
oligo-dT cellulose column (Cedarlane Labs), and the cDNA was synthesized
(Superscript II; Life Technologies, Inc.), ligated into ÀZAP phage (Strat-
agene), and screened with GAPIS on Hybond-N membrane (Amersham),
according to the manufacturer.
5' rapid amplification of cDNA ends was used to obtain the 5' end of spgp
using the Matchmaker protocol (Clontech). Spgp-specific primers 5'-
GAAAAAGTCCCAAGGAGCTGGCTG-3' and 5'-ACCCACACATAGC-
CGTCG-3' were used in the first and second amplifications, respectively.
Independent PCRs resulted in a fragment of 1 kb in length, which was
subcloned as a 900-bp Noti-Sali fragment. Two independent PCR fragments
were completely sequenced, and a third and fourth clone were also sequenced
at one position of difference to determine the correct sequence. The full-length
cDNA was cloned by ligating this fragment with a 4.5-kb, Sall-EcoRl-cut
cDNA into the Noti and EcoRl sites of pBluescript (Stratagene).
Oligonucleotide primers were designed at ~300-bp intervals to sequence
full-length spgp on both strands from a minimum of two clones by the dideoxy
5 The sequence has been deposited with accession number AFOI0597 in GenBank.
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Research.
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