New Insights into 4-Amino-2-tri-fluoromethyl-phenyl Ester Inhibition of Cell Growth and Migration in the A549 Lung Adenocarcinoma Cell Line

Wang, Hao; Gui, Shuyu; Chen, Feihu; Zhou, Qing; Wang, Yuan

doi:10.7314/apjcp.2013.14.12.7265

Cited by 18 publications

(11 citation statements)

References 40 publications

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“…4-Amino-2-trifluoromethyl-phenyl retinate (ATPR), a novel retinoid derivative synthesized by our group, inhibits proliferation and induces differentiation in many cancer cells, 11 , 12 including the ER-positive BC cell line MCF-7. 13 However, the effects of ATPR on ER-negative cells and whether CRABP2 and FABP5 expression mediates the effects of ATPR are still unclear.…”

Section: Introductionmentioning

confidence: 99%

4-Amino-2-trifluoromethyl-phenyl retinate inhibits proliferation, invasion, and migration of breast cancer cells by independently regulating CRABP2 and FABP5

Ju¹,

Wang²,

Wang³

et al. 2018

DDDT

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Background4-Amino-2-trifluoromethyl-phenyl retinate (ATPR), a novel retinoid derivative, inhibits proliferation and induces differentiation in many cancer cells. In this study, the inhibitory effects of ATPR on the proliferation, invasion, and migration of breast cancer (BC) cells, and the relationship between ATPR and the expression of the intracellular lipid-binding proteins CRABP2 and FABP5 were investigated.MethodsCRABP2 and FABP5 expression was evaluated in infiltrating breast-infiltrating ductal carcinoma(BIDC) and benign breast fibroma (BBF) by immunohistochemistry and in MCF-7, MDA-MB-231, MDA-MB-435, and MDA-MB-453 cells by immunofluorescence. The inhibition of proliferation by ATPR in these cells was detected by MTT. After downregulation and upregulation of CRABP2 and FABP5 in MCF-7 or MDA-MB-231 cells using siRNA and plasmids, the effect of ATPR on proliferation was detected by MTT and real-time cell analysis, and the effects of ATPR on the invasion and migration of MDA-MB-231 cells were detected using a Boyden chamber assay and a wound healing assay.ResultsCRABP2 expression was moderately or strongly positive in BIDC and BBF. FABP5 expression was also moderately or strongly positive in BIDC, but weakly positive or negative in BBF. CRABP2 and FABP5 were highly expressed in MCF-7 cells, moderately expressed in MDA-MB-453 cells, and weakly expressed in MDA-MB-435 and MDA-MB-231 cells. ATPR inhibited proliferation more strongly in MCF-7 cells than in other cells. The inhibition of proliferation by ATPR depended on an increase in CRABP2, but not FABP5 expression. A decrease in FABP5 could inhibit the invasion and migration of BC cells.ConclusionThese findings indicate that ATPR might inhibit proliferation by upregulating CRABP2, and inhibit invasion and migration by downregulating FABP5 in BC cells. These findings may facilitate the use of differentiation therapy in BC.

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Section: Introductionmentioning

confidence: 99%

4-Amino-2-trifluoromethyl-phenyl retinate inhibits proliferation, invasion, and migration of breast cancer cells by independently regulating CRABP2 and FABP5

Ju¹,

Wang²,

Wang³

et al. 2018

DDDT

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“…4-Amino-2-trifluoromethyl-phenyl retinate (ATPR), designed and synthesized by the College of Pharmacy, Anhui Medical University, is a novel retinoid derivative with lower toxicity than ATRA. our previous studies revealed that ATPR was superior to ATRA in terms of inhibiting cellular migration as well as promoting apoptosis and differentiation in lung, breast or gastric cancer cell lines (44)(45)(46). However, the effects of ATPR on HepG2 cell proliferation remain unknown.…”

Section: Introductionmentioning

confidence: 99%

A novel all-trans retinoic acid derivative 4-amino-2-trifluoromethyl-phenyl retinate inhibits the proliferation of human hepatocellular carcinoma HepG2 cells by inducing G0/G1 cell cycle arrest and apoptosis via upregulation of p53 and ASPP1 and downregulation of iASPP

et al. 2016

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4-Amino-2-trifluoromethyl-phenyl retinate (ATPR), a novel all-trans retinoic acid (ATRA) derivative, was reported to function as a tumor inhibitor in various types of cancer cells in vitro. However, little is known concerning its antitumor effect on human hepatocellular carcinoma (HCC) HepG2 cells. The aims of the present study were to investigate the effects of ATPR on the proliferation of HepG2 cells and to explore the probable mechanisms. A series of experiments were performed following the treatment of HepG2 cells with ATRA and ATPR. MTT and plate colony formation assays were used to measure the cell viability. To confirm the influence on proliferation, flow cytometry was used to detect the distribution of the cell cycle. Apoptosis was observed by Hoechst staining and flow cytometry. In addition, to characterize the underlying molecular mechanisms, immunofluorescence was applied to observe the distribution of p53. The transcription and translation levels of p53 were analyzed by real-time quantitative RT-PCR (qRT-PCR) and western blotting. The expression levels of murine double minute 2 (MDM2), apoptosis stimulating proteins of p53 (ASPP), cell cycle- and apoptosis-associated proteins were detected by western blotting. After HepG2 cells were incubated with ATRA and ATPR, the viability of the HepG2 cells was inhibited in a dose- and time-dependent manner. As well, ATPR significantly suppressed HepG2 cell colony formation and arrested cells at the G0/G1 phase, while ATRA had no obvious effects. Both Hoechst staining and flow cytometry unveiled the apoptosis of HepG2 cells. Moreover, the fluorescent density of p53 was higher in the nuclei after exposure to ATPR than that in the ATRA group. HepG2 cells treated with ATPR showed elevated mRNA and protein levels of p53 when compared with these levels in the ATRA-treated cells. Western blotting showed that ATPR increased ASPP1, p21 and Bax expression and decreased MDM2, iASPP, cyclin D and E, cyclin-dependent kinase 6 (CDK6) and Bcl-2 expression, while CDK4 and ASPP2 expression were scarcely altered. Consequently, ATPR exerted a better inhibitory effect on the proliferation of HepG2 cells than ATRA through increased expression of p53 and ASPP1 and downregulation of iASPP, thereby resulting in G0/G1 cell cycle arrest and apoptosis.

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“…Adenocarcinoma cannot be treated adequately through simple operations. Therefore, chemotherapy remains the mainstay treatments for lung cancer (Wang et al, 2013;Zhou et al, 2014). Cisplatin, as the first line drug, is extensively applied for the clinical treatment of nonsmall-cell lung cancer (Fan and Jiang, 2008).…”

Section: Introductionmentioning

confidence: 99%

Regulatory Mechanisms of Annexin-Induced Chemotherapy Resistance in Cisplatin Resistant Lung Adenocarcinoma

Wang

Xiao²,

Li³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Adenocarcinoma of lung has high incidence and a poor prognosis, woith chemotherapy as the main therapeutic tool, most commonly with cisplatin. However, chemotherapy resistance develops in the majority of patients during clinic treatment. Mechanisms of resistance are complex and still unclear. Although annexin play important roles in various tumor resistance mechanisms, their actions in cisplatin-resistant lung adenocarcinoma remain unclear. Preliminary studies by our group found that in cisplatin-resistant lung cancer A549 cells and lung adenocarcinoma tissues, both mRNA and protein expression of annexins A1, A2 and A3 is increased. Using a library of annexin A1, A2 and A3 targeting combined molecules already established by ourselves we found that specific targeting decreased cisplatin-resistance. Taken together, the underlined effects of annexins A1, A2 and A3 on drug resistance and suggest molecular mechanisms in cisplatin-resistant A549 cells both in vivo and in vitro. Furthermore, the study points to improved research on occurrence and development of lung adenocarcinoma, with provision of effective targets and programmes for lung adenocarcinoma therapy in the clinic.

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New Insights into 4-Amino-2-tri-fluoromethyl-phenyl Ester Inhibition of Cell Growth and Migration in the A549 Lung Adenocarcinoma Cell Line

Cited by 18 publications

References 40 publications

4-Amino-2-trifluoromethyl-phenyl retinate inhibits proliferation, invasion, and migration of breast cancer cells by independently regulating CRABP2 and FABP5

4-Amino-2-trifluoromethyl-phenyl retinate inhibits proliferation, invasion, and migration of breast cancer cells by independently regulating CRABP2 and FABP5

A novel all-trans retinoic acid derivative 4-amino-2-trifluoromethyl-phenyl retinate inhibits the proliferation of human hepatocellular carcinoma HepG2 cells by inducing G0/G1 cell cycle arrest and apoptosis via upregulation of p53 and ASPP1 and downregulation of iASPP

Regulatory Mechanisms of Annexin-Induced Chemotherapy Resistance in Cisplatin Resistant Lung Adenocarcinoma

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