Prooxidative activity of plumbagin induces apoptosis in human pancreatic ductal adenocarcinoma cells via intrinsic apoptotic pathway

Pandey, Kamal; Tripathi, Surya Kant; Panda, Munmun; Biswal, Bijesh K.

doi:10.1016/j.tiv.2020.104788

Cited by 19 publications

(6 citation statements)

References 22 publications

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“…As a natural quinone, plumbagin exhibits various biological activities, such as antibacterial [ 29 ], immunomodulatory [ 30 ] and pro-oxidative stress [ 31 ] activities. The anti-cancer effects of plumbagin have been shown in pancreatic cancer [ 32 ], liver cancer [ 33 ], oesophageal cancer [ 34 ], gastric cancer [ 35 ] and other digestive system tumours. Plumbagin also promoted apoptosis in colon cancer cells [ 36 ].…”

Section: Discussionmentioning

confidence: 99%

Plumbagin induces ferroptosis in colon cancer cells by regulating p53-related SLC7A11 expression

Wang,

Kong,

et al. 2024

Heliyon

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Section: Discussionmentioning

confidence: 99%

Plumbagin induces ferroptosis in colon cancer cells by regulating p53-related SLC7A11 expression

Wang,

Kong,

et al. 2024

Heliyon

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“…22, 23 Plumbagin data on pancreatic cancer cells showed that it activated apoptosis through the induction of ROS production along with upregulation of cleaved caspase 3 and caspase 9 and downregulation of Bcl-2 protein. 24 The caspase cascade is the key signaling pathway that triggered apoptosis. 25 Therefore, plumbagin activate apoptosis may be beneficial for anticancer treatment including CCA cells.…”

Section: Discussionmentioning

confidence: 99%

Plumbagin Suppresses Growth, Induces Apoptosis, and Inhibits Migration in Cholangiocarcinoma via Reactive Oxygen Species Generation and Mitochondrial Function

Buranrat

Utsintong

2023

Pharmacognosy Magazine

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Objectives: Plumbagin has been displayed on growth inhibition in several cancer cells; however, the anticancer effects of plumbagin on cholangiocarcinoma (CCA) cell are still less information. This article will explore the potential anticancer effects and underlying mechanisms of plumbagin on CCA cells. Materials and Methods: Two types of CCA cell, including KKU-100 with slow growth and migration and KKU-M452 with rapid growth and migration, were treated with plumbagin and measured the growth inhibition and migratory suppression by sulforhodamine B, colony formation, acridine orange/ethidium bromide staining, wound healing, and Matrigel migration. Apoptosis induction, reactive oxygen species (ROS) formation, and mitochondrial function were analyzed by the flow cytometric method. Results: To compare the plumbagin effects on two types of CCA cells, the data indicated that plumbagin strongly reduced cell proliferation in a concentration- and time-dependent manner. At 72 h, IC50 values were 1.11 ± 0.12 µM for KKU-100 and 2.52 ± 0.40 µM for KKU-M452 cells, with inhibition of the cell cycle in the G0/G1 phase for KKU-100 and the G2/M phase for KKU-M452, respectively. Moreover, plumbagin decreased cell migration in both CCA cells in a dose-dependent manner. Furthermore, late apoptosis was significantly induced after treatment with plumbagin. Mechanistically, plumbagin increased ROS along with decreased mitochondrial function in CCA cells. Finally, the position of 5-hydroxy on the naphthoquinone ring of plumbagin was in a good position to form an H-bond with the amino group for all caspase 3, cytochrome C, and p21 binding sites, and these data indicated that plumbagin suppressed CCA cells via modulation of these proteins. Conclusion: Plumbagin strongly suppresses cell viability and stimulates apoptosis in CCA cells via induction of ROS and inhibition of mitochondrial function.

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“…Flow cytometry was performed as described previously [ 39 ]. This assay was performed with an Annexin V-FITC/PI Apoptosis Kit (Yeason Biotechnology, Shanghai, China).…”

Section: Methodsmentioning

confidence: 99%

Transmembrane protein 176B regulates amino acid metabolism through the PI3K-Akt-mTOR signaling pathway and promotes gastric cancer progression

Li,

Fang,

Dal

et al. 2024

Cancer Cell Int

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Background The present study aimed to investigate the expression level, biological function, and underlying mechanism of transmembrane protein 176B (TMEM176B) in gastric cancer (GC). Methods TMEM176B expression was detected by quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting (WB). The function of TMEM176B was determined by various in vitro assays including colony formation, 5-ethynyl-2ʹ-deoxyuridine (EdU), Transwell, and flow cytometry. Bioinformatics techniques were then used to elucidate the signaling pathways associated with TMEM176B activity. Tumor formation experiments were conducted on nude mice for in vivo validation of the preceding findings. TMEM176B expression was cross-referenced to clinicopathological parameters and survival outcomes. Results It was observed that TMEM176B was overexpressed in GC cells and tissues. Targeted TMEM176B abrogation inhibited colony formation, proliferation, migration, and invasion but promoted apoptosis in GC cell lines while TMEM176B overexpression had the opposite effects. Subsequent experimental validation disclosed an association between TMEM176B and the phosphatidylinositol 3-carboxykinase (PI3K)-protein kinase B (Akt)-mammalian target of rapamycin (mTOR) signaling axis. Moreover, TMEM176B affects GC cancer progression by regulating asparagine synthetase (ASNS). The in vivo assays confirmed that TMEM176B is oncogenic and the clinical data revealed a connection between TMEM176B expression and the clinicopathological determinants of GC. Conclusion The foregoing results suggest that TMEM176B significantly promotes the development of gastric cancer and is an independent prognostic factor of it.

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Prooxidative activity of plumbagin induces apoptosis in human pancreatic ductal adenocarcinoma cells via intrinsic apoptotic pathway

Cited by 19 publications

References 22 publications

Plumbagin induces ferroptosis in colon cancer cells by regulating p53-related SLC7A11 expression

Plumbagin induces ferroptosis in colon cancer cells by regulating p53-related SLC7A11 expression

Plumbagin Suppresses Growth, Induces Apoptosis, and Inhibits Migration in Cholangiocarcinoma via Reactive Oxygen Species Generation and Mitochondrial Function

Transmembrane protein 176B regulates amino acid metabolism through the PI3K-Akt-mTOR signaling pathway and promotes gastric cancer progression

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