Anti-leukemic effects of gallic acid on human leukemia K562 cells: Downregulation of COX-2, inhibition of BCR/ABL kinase and NF-κB inactivation

Reddy, T. Chandramohan; Reddy, D. Bharat; Aparna, A.; Arunasree, Kalle M.; Gupta, Geetika; Achari, Chandrani; Reddy, Gorla V.; Lakshmipathi, V.; Subramanyam, A.; Reddanna, Pallu

doi:10.1016/j.tiv.2011.12.018

Cited by 68 publications

(27 citation statements)

References 47 publications

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“…By overexpressing Cox-2 in K562 cells, Chandramohan et al . found that the CML cells are less susceptible to gallic acid-induced apoptosis, an effect attributed in part to increased expression of Bcl-2 and decreased of cytochrome c release (32). Other NSAIDs, such as aspirin, are reported to have similar pro-apoptotic effects on CLL cells.…”

Section: Inhibiting Cox-2 In Hematological Malignanciesmentioning

confidence: 99%

The Influence of Cox-2 and Bioactive Lipids on Hematological Cancers

Ramon

Woeller

Phipps

2014

CAG

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Inflammation is implicated in the progression of multiple types of cancers including lung, colorectal, breast and hematological malignancies. Cyclooxygenases (Cox) -1 and -2 are important enzymes involved in the regulation of inflammation. Elevated Cox-2 expression is associated with a poor cancer prognosis. Hematological malignancies, which are among the top 10 most predominant cancers in the USA, express high levels of Cox-2. Current therapeutic approaches against hematological malignances are insufficient as many patients develop resistance or relapse. Therefore, targeting Cox-2 holds promise as a therapeutic approach to treat hematological malignancies. NSAIDs and Cox-2 selective inhibitors are anti-inflammatory drugs that decrease prostaglandin and thromboxane production while promoting the synthesis of specialized proresolving mediators. Here, we review the evidence regarding the applicability of NSAIDs, such as aspirin, as well as Cox-2 specific inhibitors, to treat hematological malignancies. Furthermore, we discuss how FDA-approved Cox inhibitors can be used as anti-cancer drugs alone or in combination with existing chemotherapeutic treatments.

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Section: Inhibiting Cox-2 In Hematological Malignanciesmentioning

confidence: 99%

The Influence of Cox-2 and Bioactive Lipids on Hematological Cancers

Ramon

Woeller

Phipps

2014

CAG

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“…Ara-C treatment induced significant S-phase arrest in THP-1/Ctrl cells, while THP-1/miR-99a cells showed less S-phase arrest 24 hrs post treatment compared to untreated cells (Figure 2D, 3D). Different from Ara-C, imatinib can induce cell cycle arrest at G1 phase [26], and K562/miR-99a cells still showed less G1 arrest compared to K562/Ctrl cells after treated with imatinib for 24 hrs (Figure 2D, 3D). However, the results of apoptosis analyses showed no significant difference between miR-99a and Ctrl cells after exposure to these chemotherapeutic agents (Figure S3).…”

Section: Resultsmentioning

confidence: 99%

Upregulation of miR-99a is associated with poor prognosis of acute myeloid leukemia and promotes myeloid leukemia cell expansion

Zhang

Xing

et al. 2016

Oncotarget

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Leukemia stem cells (LSCs) can resist available treatments that results in disease progression and/or relapse. To dissect the microRNA (miRNA) expression signature of relapse in acute myeloid leukemia (AML), miRNA array analysis was performed using enriched LSCs from paired bone marrow samples of an AML patient at different disease stages. We identified that miR-99a was significantly upregulated in the LSCs obtained at relapse compared to the LSCs collected at the time of initial diagnosis. We also found that miR-99a was upregulated in LSCs compared to non-LSCs in a larger cohort of AML patients, and higher expression levels of miR-99a were significantly correlated with worse overall survival and event-free survival in these AML patients. Ectopic expression of miR-99a led to increased colony forming ability and expansion in myeloid leukemia cells after exposure to chemotherapeutic drugs in vitro and in vivo, partially due to overcoming of chemotherapeutic agent-mediated cell cycle arrest. Gene profiling and bioinformatic analyses indicated that ectopic expression of miR-99a significantly upregulated genes that are critical for LSC maintenance, cell cycle, and downstream targets of E2F and MYC. This study suggests that miR-99a has a novel role and potential use as a biomarker in myeloid leukemia progression.

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“…GSH depletion is another mechanism by which it prevents cancer cell growth and induces apoptosis . Gallic acid also reduces the leukemic cell growth by inducing the cell cycle arrest . In imatinib‐resistant human leukemia K562 cells, gallic acid inhibits cyclooxygenase‐2, BCR/ABL kinase, and NFκB activation, and thereby suppressing the cell proliferation .…”

Section: Gallates Induces Mitochondrial Pathway Of Apoptosis In Cancementioning

confidence: 99%

“…Gallic acid also reduces the leukemic cell growth by inducing the cell cycle arrest . In imatinib‐resistant human leukemia K562 cells, gallic acid inhibits cyclooxygenase‐2, BCR/ABL kinase, and NFκB activation, and thereby suppressing the cell proliferation . Gallic acid is auto‐oxidized to form superoxides and H 2 O 2 , which dissipates the mitochondrial membrane potential and stimulates apoptosis as observed in prostate cancer cells .…”

Section: Gallates Induces Mitochondrial Pathway Of Apoptosis In Cancementioning

confidence: 99%

Gallic Acid and Gallates in Human Health and Disease: Do Mitochondria Hold the Key to Success?

Kosuru

Roy

Das

et al. 2017

Molecular Nutrition Food Res

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Gallic acid and gallate esters are widely used as dietary supplements or additives with clinical significances. Over the last few decades, a large number of publications have been reported stating the antioxidative, antiapoptotic, cardioprotective, neuroprotective, and anticancer properties of gallic acid and gallates, and mostly demonstrated their antioxidative or prooxidative properties influencing the reactive oxygen species (ROS) signaling networks. However, very little focus has been paid to clinical trials, and this restricted their use as a prescribed preventative supplement. Since mitochondria are the principal organelles responsible for ROS generation, we reviewed the existing literature of mitochondria-specific effects of gallates including ROS production, respiration, mitochondrial biogenesis, apoptosis, and the physico-chemical parameters affecting the outcome of gallate supplementation to various health scenarios such as cardiovascular diseases, neurodegeneration, hepatic ailments, or cancers. The major signaling pathways and the molecules targeted by gallic acid and its derivatives have also been discussed with emphasis on mitochondria as the target site. This review provides a better understanding of the effect of gallic acid and gallate esters on mitochondrial functions and in designing effective preventative measures against the onset of various diseases.

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Anti-leukemic effects of gallic acid on human leukemia K562 cells: Downregulation of COX-2, inhibition of BCR/ABL kinase and NF-κB inactivation

Cited by 68 publications

References 47 publications

The Influence of Cox-2 and Bioactive Lipids on Hematological Cancers

The Influence of Cox-2 and Bioactive Lipids on Hematological Cancers

Upregulation of miR-99a is associated with poor prognosis of acute myeloid leukemia and promotes myeloid leukemia cell expansion

Gallic Acid and Gallates in Human Health and Disease: Do Mitochondria Hold the Key to Success?

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