Role of gambogic acid and NaI131 in A549/DDP cells

Huang, Jing; Zhu, Xiaoyun; Wang, Huan; Han, Shuhua; Lü, Ling; Xie, Yan; Chen, Daozhen; Zhang, Qiang; Zhang, Li; Hu, Yue

doi:10.3892/ol.2016.5435

Cited by 10 publications

(13 citation statements)

References 54 publications

(51 reference statements)

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“…3 Numerous studies indicated that GA acted as the suppressor of cancers, including GC. 3 , 4 For example, Wang et al indicated that GA could increase docetaxel sensitivity in GC cells. 5 Zou et al revealed that GA induced cell apoptosis together with chemotherapeutic agents in GC cells.…”

Section: Introductionmentioning

confidence: 99%

<p>Gambogic Acid Inhibits the Progression of Gastric Cancer via circRNA_ASAP2/miR-33a-5p/CDK7 Axis</p>

Lin¹,

Lin²,

He³

et al. 2020

CMAR

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Background: Gastric cancer (GC) is a major cancer-related mortality disease. Gambogic acid (GA) has been investigated to inhibit cancer progression. In the present study, the molecular mechanism of GA in regulating GC progression was studied. Methods: The expression levels of circular RNA ASAP2 (circ_ASAP2), miR-33a-5p and cyclin-dependent kinases 7 (CDK7) were detected by quantitative real-time polymerase reaction (qRT-PCR). CDK7 protein level was evaluated by Western blot. Cell colony formation assay, 3-(4,5-Dimethylthazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, transwell assay and flow cytometry analysis were employed to reveal the functional effects among circ_ASAP2, miR-33a-5p and CDK7 on GA-induced GC progression. Mechanistically, the binding relationship between miR-33a-5p and circ_ASAP2 or CDK7 was predicted with starBase v3.0 online database and verified by dual-luciferase reporter assay. In vivo tumor formation assay was used to explain the impacts of GA treatment on GC growth in vivo. Results: Circ_ASAP2 and CDK7 expression were downregulated in GA-induced GC cells compared with GC cells. MiR-33a-5p expression was upregulated in GA-induced GC cells relative to GC cells. The protein expression level of CDK7 was lower in GA-induced GC cells than that in GC cells. Further, circ_ASAP2 overexpression decreased GA-induced inhibition effects on cell proliferation, migration and invasion and GA-induced promotion effect on cell apoptosis in both AGS and HGC-27 cells, whereas this phenomenon was reversed by miR-33a-5p. In addition, circ_ASAP2 functioned as a sponge of miR-33a-5p and miR-33a-5p was associated with CDK7. Furthermore, GA treatment inhibited GC growth in vivo. Conclusion: Circ_ASAP2 overexpression promoted cell proliferation, migration and invasion, whereas inhibited cell apoptosis by upregulating CDK7 expression through binding to miR-33a-5p in GA-induced GC cells. This study provided a theoretical basis in GC treatment with GA.

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Section: Introductionmentioning

confidence: 99%

<p>Gambogic Acid Inhibits the Progression of Gastric Cancer via circRNA_ASAP2/miR-33a-5p/CDK7 Axis</p>

Lin¹,

Lin²,

He³

et al. 2020

CMAR

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“…Members of the Bcl-2 family are key regulators of mitochondria-related apoptosis [ 3 , 8 ], and an imbalance in expression of anti-apoptotic Bcl-xL or Bcl-2 and pro-apoptotic Bax leads to apoptosis; therefore, the Bax/Bcl-xL or Bax/Bcl-2 ratio is an important indicator of apoptosis [ 3 , 15 , 43 , 44 ]. Many studies have shown that the Bax/Bcl-2 ratio is the main factor for apoptosis induction in cancers such as breast, prostate, liver and lung cancer [ 4 , 16 , 18 , 42 ]. The Bax/Bcl-xL ratio is also associated with induction of apoptosis in several cancer cell lines, such as pancreatic neoplasia and mesothelioma cells [ 19 , 31 ].…”

Section: Discussionmentioning

confidence: 99%

Photodynamic Therapy Using a Novel Phosphorus Tetraphenylporphyrin Induces an Anticancer Effect via Bax/Bcl-xL-related Mitochondrial Apoptosis in Biliary Cancer Cells

Huynh

Yamaguchi

Choijookhuu

et al. 2020

Acta Histochem. Cytochem

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Photodynamic therapy (PDT) uses photosensitizer activation by light of a specific wavelength, and is a promising treatment for various cancers; however, the detailed mechanism of PDT remains unclear. Therefore, we investigated the anticancer effect of PDT using a novel phosphorus tetraphenylporphyrin (Ptpp) in combination with light emitting diodes (Ptpp-PDT) in the NOZ human biliary cancer cell line. Cell viability and apoptosis were examined by MTT assay, flow cytometry and TUNEL assay for 24 hr after Ptpp-PDT. MitoTracker and JC-1 were used as markers of mitochondrial localization and membrane potential. The levels of mitochondrial oxidative phosphorylation (OXPHOS) complexes, Bcl-2 family proteins, cytochrome c and cleaved caspase-3 were examined by western blotting and immunohistochemistry. The results revealed that Ptpp localized to mitochondria, and that Ptpp-PDT efficiently decreased cell viability in a dose- and time-dependent manner. JC-1 and OXPHOS complexes decreased, but apoptotic cells increased from 6 to 24 hr after Ptpp-PDT. A decrease in Bcl-xL and increases in Bax, cytochrome c and cleaved caspase-3 were also found from 6 to 24 hr after Ptpp-PDT. Based on these results, we conclude that Ptpp-PDT induces anticancer effects via the mitochondrial apoptotic pathway by altering the Bax/Bcl-xL ratio, and could be an effective treatment for human biliary cancer.

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“…5 × 10 4 cells per well were seeded in 6-well plates and cultured at 37℃, 5% CO 2 for 24 h and divided into the NaI 131 group, GA group, combination group and control group. The NaI 131 group was treated with 10.3 MBq NaI 131 , the GA group with 2.9 µg/ml GA, and the combination group with 10.3 MBq NaI 131 and 0.3 µg/ml GA as described previously [23]. The control group was treated with PBS (2 ml per well).…”

Section: Cell Culturementioning

confidence: 99%

“…We rst tested whether the combination treatment may have effect on cell cycle, since our previous results showed that treatment of A549/DDP cells with low-dose GA together with NaI 131 was able to signi cantly inhibit cell proliferation. [23] NaI 131 , GA, and a combination of both were used to treat A549, A549/DDP, and A549/Taxol cells and control group was treated with PBS. The cell cycle conditions in all groups were observed after 48 h (Fig.…”

Section: Analysis Of Stages In the Cell Cyclementioning

confidence: 99%

“…[22] Our previous results showed that a combination of low-dose GA and NaI 131 was able to signi cantly inhibit cell proliferation as well as induce cell apoptosis in A549/DDP cells. [23] Therefore, we aimed to further study the plausible cellular mechanisms related to the effect of the combination therapy on two drug-resistant lung cancer cell lines. Additionally, we also explored if the combination therapy conferred inhibition to therapy resistance in NSCLC, so as to achieve better therapeutic results.…”

Section: Introductionmentioning

confidence: 99%

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Combined effects of low-dose gambogic acid and NaI131 in drug-resistant non-small-cell lung cancer cells

Huang

Ding

et al. 2020

Preprint

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Background Radioactive seed is a method for treating drug-resistant, late-stage non-small cell lung cancer (NSCLC), but has undesirable side effects. Gambogic acid (GA), an ingredient of traditional Chinese medicine, exerts broad-spectrum antitumour activities via several pathways. This study aimed to elucidate the mechanism involved in the combined effect of low-dose GA and NaI131 to sensitize the antitumour activity of NaI131 in drug-resistant NSCLC cells. Methods Human NSCLC cell line A549 and drug-resistant cell lines A549/DDP and A549/Taxol were treated with NaI131, low-dose GA or a combination of both; control group of each cell line was treated with phosphate-buffered saline. Following treatment, cell proliferation, apoptosis, cell cycle, and levels of expression of apoptosis-related proteins namely CDK1, Cyclin B, mtp53, HSP90, and Bax, Bcl-2 respectively, and P-glycoprotein 1 (P-gp) known to confer resistance to chemotherapy, were detected using western blotting and immunofluorescence. mRNA levels of mtp53 and HSP90 were measured using qRT-PCR. Results Compared to the control group, A549, A549/DDP, and A549/Taxol cells treated with NaI131, GA or combination of drugs exhibited G2/M arrest, increased percentage of total apoptotic cells, significantly reduced protein levels of CDK1, Cyclin B, mtp53, HSP90, Bcl-2 and P-gp, increased protein levels of Bax and decreased mRNA levels of mtp53 and HSP90. The changes in the combination group were significantly different from the other groups. Conclusion In NSCLC cell lines, low-dose GA could enhance the effect of NaI131 on G2/M arrest, promote cell apoptosis, reduce drug-resistance and hence could be explored as a potential radionuclide sensitizer.

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Role of gambogic acid and NaI131 in A549/DDP cells

Cited by 10 publications

References 54 publications

<p>Gambogic Acid Inhibits the Progression of Gastric Cancer via circRNA_ASAP2/miR-33a-5p/CDK7 Axis</p>

<p>Gambogic Acid Inhibits the Progression of Gastric Cancer via circRNA_ASAP2/miR-33a-5p/CDK7 Axis</p>

Photodynamic Therapy Using a Novel Phosphorus Tetraphenylporphyrin Induces an Anticancer Effect via Bax/Bcl-xL-related Mitochondrial Apoptosis in Biliary Cancer Cells

Combined effects of low-dose gambogic acid and NaI131 in drug-resistant non-small-cell lung cancer cells

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