Retinoic acid and interferon combination studies in human cancer

Lippman, Scott M.; Glisson, Bonnie S.; Kavanagh, John J.; Lotan, Reuben; Hong, Waun Ki; Paredes-Espinoza, Mario; Hittelman, Walter N.; Holdener, E. E.; Krakoff, Irwin H.

doi:10.1016/0959-8049(93)90618-p

Cited by 44 publications

(29 citation statements)

References 49 publications

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“…Their published findings may support our present observations. Retinoids are now used as a chemopreventive or chemotherapeutic agent for patients with several solid tumours Lippman et al, 1993;Mitchell et al, 1995). Furthermore, a triple combination of 5-fluorouracil, vitamin A and cobalt-60 radiation, so-called FAR therapy, has been applied to treat the patients with head and neck tumours (Komiyama et al, 1978).…”

Section: Discussionmentioning

confidence: 99%

“…The effects of retinoids are mediated by both nuclear retinoid receptors (RARs and RXRs) and cytoplasmic retinoic acid binding proteins (CRABP1 and CRABP2) (Pemrick et al, 1994). Retinoids are used as a chemopreventive or chemotherapeutic agent for patients with several solid tumours, and some successful results from the clinical trials has been reported Lippman et al, 1993;Mitchell et al, 1995). Hong et al (1990) reported that 13-cis retinoic acid (13-cisRA) suppressed the oral pre-malignant lesions and decreased the incidence of second primary tumours in head and neck cancer.…”

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Low-dose retinoic acid enhances in vitro invasiveness of human oral squamous-cell-carcinoma cell lines

et al. 2001

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Summary Retinoids inhibit the proliferation of several types of tumour cells, and are used for patients with several malignant tumours. In this study, we examined the effect of retinoic acids (RAs) on the invasive potentials of the oral squamous cell carcinoma (SCC) cells, BHY and HNt. BHY cells expressed all of retinoid nuclear receptors (RARα, β, γ, and RXRα) and cytoplasmic retinoic acid binding proteins (CRABP1 and CRABP2). HNt cells lacked the expression of RARβ, but expressed other nuclear receptors and CRABPs. All-trans retinoic acid (ATRA) and 13-cis retinoic acid (13-cisRA) (10 -6 and 10 -7 M) inhibited the growth of the cells, but low-dose ATRA and 13-cisRA (10 -8 M) marginally affected the growth of the cells. Surprisingly, low-dose RAs enhanced the activity of tissue-type plasminogen activator (tPA), and activated pro-matrix metalloproteinases (proMMP2 and proMMP9). Activation of proMMP2 and proMMP9 was inhibited by aprotinin, a serineproteinase, tPA inhibitor. MATERIALS AND METHODS Cells and cell cultureBHY and HNt (Kawamata et al, 1997) cells were derived from human oral SCC tumours from patients. HT1080 cells are a human fibrosarcoma cell line purchased from Dai-Nippon Seiyaku, Osaka, Japan. All of the cells were maintained in DMEM (Life Technologies, Inc, Gaithersburg, MD) supplemented with 10% FCS (Bio-Whittaker, Walkersville, MD), 100 µg ml -1 streptomycin, and 100 U ml -1 penicillin, 0.25 µg ml -1 Amphotericin B (Life Technologies, Inc.) in a humidified atmosphere of 95% air and 5% CO 2 at 37˚C. MTT assayWe examined the effect of ATRA (Sigma, St. Louis, MO) and 13-cisRA (Sigma) on the growth of the cells by an assay in which MTT (Sigma) was used. Cells were seeded on a 96-well plate (Falcon; Becton Dickinson Labware, Lincoln Park, NJ) at 5 × 10 3 cells per well in DMEM containing 10% FCS. After 24 h, cells were washed twice with DMEM without FCS and cultured in DMEM without FCS in the presence or absence of ATRA (10 -6 , 10 -7 and 10 -8 M) or 13-cisRA (10 -6 , 10 -7 and 10 -8 M). After 3 days, the number of cells was quantitated by MTT assay (Carmichael et al, 1987). Gelatinase zymography and reverse gelatinase zymographyCells were grown to confluence in 60 mm dishes (Falcon) in the serum-supplemented medium, washed twice with serum-free DMEM, and cultured in 3 ml of serum-free DMEM in the presence or absence of ATRA (10 -8 M) or 13-cisRA (10 -8 M) for an additional 48 h. The medium was collected, clarified by centrifugation at 1800 g, and concentrated down to 0.1 ml approximately 30-fold by Centricon 10 (cut-off, Mr 10 000; Millipore Corp, Bedford, MA). We have already confirmed that the process of the protein concentration did not activate the progelatinases in the samples (Kawamata et al, 1997). The protein concentration of the samples are determined by Bio-Rad protein assay (Bio-Rad, Hercules, CA). The gels for zymorgraphy were composed of gelatin (0.1%; Sigma) and polyacrylamide (10%), and for reverse zymography, of gelatin (0.1%), polyacrylamide (12.5%) and concentrated conditioned medi...

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Section: Discussionmentioning

confidence: 99%

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Low-dose retinoic acid enhances in vitro invasiveness of human oral squamous-cell-carcinoma cell lines

et al. 2001

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“…Although IFNs and retinoids have been shown to suppress the growth of certain tumor cells, a number of tumor cells are not inhibited by these single agents (6,7). However, a combination of these agents produces significant additive or synergistic anti-tumor activity (7,8).…”

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Modulation of Interferon (IFN)-inducible Gene Expression by Retinoic Acid

Kolla

Lindner

Xiao

et al. 1996

Journal of Biological Chemistry

115

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“…33,34 It has been shown that IFNs induce retinoic acid receptors in acute promyelocytic leukemia cells and cooperate with RA to overcome the resistance of cells to RA. 36,52 Also RA activates interferon regulatory factor-1 gene expression in promyelocytic leukemia cells.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have suggested that RA and IFNs have synergistic effects on cellular differentiation. 33,34 They have been used as a combination therapy with encouraging results, in certain forms of cancer such as squamous cell carcinoma of the skin and cervix. 35 Whether such combination therapy has potential in other cancers is not known.…”

Section: Introductionmentioning

confidence: 99%

Interferons and retinoids enhance and dexamethasone suppresses urokinase-mediated plasminogen activation in promyelocytic leukemia cells

et al. 1998

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All-trans retinoic acid (RA) has been successfully used in the treatment of patients with acute promyelocytic leukemia (APL). It induces differentiation of APL cells and reduces the bleeding tendency in APL patients. It has been proposed that plasminogen activation could affect the fibrinolytic balance in patients with leukemia. In our earlier study we found that treatment of APL cells with RA results in changes in urokinase (uPA) production. As interferons (IFNs) and dexamethasone can be used together with RA in the treatment of patients with APL, we have now studied the effects of RA together with IFNs and dexamethasone on the plasminogen activation cascade of these cells, including measurement of plasmin generation and uPA receptor (uPAR), using enzyme immunoassays, fluorescence-activated cell sorter analysis and RNA extraction with Northern blotting. Our main results were: (1) plasmin was formed on the surface of APL cells; (2) RA stimulated transiently plasmin generation and increased uPAR mRNA level; (3) IFNs ␣ and ␥ potentiated RA in its effects on uPA and plasmin activities and on uPAR level; (4) dexamethasone suppressed totally the effect of RA on uPA induction and plasminogen activation; and (5) IFNs and dexamethasone alone did not have potent effects on plasminogen activation. These results may assist in the design of therapy for APL patients.

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Retinoic acid and interferon combination studies in human cancer

Cited by 44 publications

References 49 publications

Low-dose retinoic acid enhances in vitro invasiveness of human oral squamous-cell-carcinoma cell lines

Low-dose retinoic acid enhances in vitro invasiveness of human oral squamous-cell-carcinoma cell lines

Modulation of Interferon (IFN)-inducible Gene Expression by Retinoic Acid

Interferons and retinoids enhance and dexamethasone suppresses urokinase-mediated plasminogen activation in promyelocytic leukemia cells

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