The Application of Arsenic Trioxide in Ameliorating ABT-737 Target Therapy on Uterine Cervical Cancer Cells through Unique Pathways in Cell Death

Hsin, I.; Chou, Ying-Hsiang; Hung, Wei-Li; Wang, Po-Hui

doi:10.3390/cancers12010108

Cited by 14 publications

(10 citation statements)

References 48 publications

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“…The fixed cells were stained with propidium iodine, and cell cycle distribution was analyzed by flow cytometry. The complete protocol for both analyses has been described elsewhere [ 14 ].…”

Section: Methodsmentioning

confidence: 99%

Suppression of PI3K/Akt/mTOR/c-Myc/mtp53 Positive Feedback Loop Induces Cell Cycle Arrest by Dual PI3K/mTOR Inhibitor PQR309 in Endometrial Cancer Cell Lines

Hsin

Shen

Chang

et al. 2021

Cells

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Gene mutations in PIK3CA, PIK3R1, KRAS, PTEN, and PPP2R1A commonly detected in type I endometrial cancer lead to PI3K/Akt/mTOR pathway activation. Bimiralisib (PQR309), an orally bioavailable selective dual inhibitor of PI3K and mTOR, has been studied in preclinical models and clinical trials. The aim of this study is to evaluate the anticancer effect of PQR309 on endometrial cancer cells. PQR309 decreased cell viability in two-dimensional and three-dimensional cell culture models. PQR309 induced G1 cell cycle arrest and little cell death in endometrial cancer cell lines. It decreased CDK6 expression and increased p27 expression. Using the Proteome Profiler Human XL Oncology Array and Western blot assay, the dual inhibitor could inhibit the expressions of c-Myc and mtp53. KJ-Pyr-9, a c-Myc inhibitor, was used to prove the role of c-Myc in endometrial cancer survival and regulating the expression of mtp53. Knockdown of mtp53 lowered cell proliferation, Akt/mTOR pathway activity, and the expressions of c-Myc. mtp53 silence enhanced PQR309-inhibited cell viability, spheroid formation, and the expressions of p-Akt, c-Myc, and CDK6. This is the first study to reveal the novel finding of the PI3K/mTOR dual inhibitor in lowering cell viability by abolishing the PI3K/Akt/mTOR/c-Myc/mtp53 positive feedback loop in endometrial cancer cell lines.

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Section: Methodsmentioning

confidence: 99%

Suppression of PI3K/Akt/mTOR/c-Myc/mtp53 Positive Feedback Loop Induces Cell Cycle Arrest by Dual PI3K/mTOR Inhibitor PQR309 in Endometrial Cancer Cell Lines

Hsin

Shen

Chang

et al. 2021

Cells

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“…The HeLa cells (7 × 10 4 cells/well) and SiHa cells (7 × 10 4 cells/well) were seeded in a 24‐well plate with 100 μl of the culture medium. The medium was removed after 24 h of culturing, and 100 μl of a medium containing 0.5 mg/ml MTT was applied 26 …”

Section: Methodsmentioning

confidence: 99%

CLEFMA induces intrinsic and extrinsic apoptotic pathways through ERK1/2 and p38 signalling in uterine cervical cancer cells

Lee

Hsiao

Chen

et al. 2023

J Cellular Molecular Medi

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“…The proposed mechanism is that arsenic trioxide reduces anti-apoptotic protein Mcl-1 in Caski cells and enhancement of ABT-737-induced apoptosis and caspase-7 activation. 74 These suggested that ABT-737 and related BH3 mimetic drugs, in combination or alone, may be of value as a new therapeutic option for dedifferentiated thyroid carcinomas. ABT-737 also appears to work through triggering platelet phosphatidylserine in a caspase-dependent manner.…”

Section: New Therapeutic Agents and Novel Drug Targetmentioning

confidence: 99%

A recent development of new therapeutic agents and novel drug targets for cancer treatment

et al. 2021

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Despite recent advances in cancer diagnosis, prevention, detection, as well as management, the disease is expected to be the top cause of death globally. The chemotherapy approach for cancer has become more advanced in its design, yet no medication can cure enough against all types of cancer and its stage. Thus, this review aimed to summarize a recent development of new therapeutic agents and novel drug targets for the treatment of cancer. Several obstacles stand in the way of effective cancer treatment and drug development, including inaccessibility of tumor site by appropriate drug concentration, debilitating untoward effects caused by non-selective tissue distribution of chemotherapeutic agents, and occurrence of drug resistance, which leads to cross-resistance to a variety of drugs. Resistance to treatment with anticancer drugs results from multiple factors and the most common reason for acquiring drug resistance is marking and expelling drugs that prevent cancer cells to be targeted by chemotherapeutic agents. Moreover, insensitivity to drug-induced apoptosis, alteration, and mutation of drug target and interference/change of DNA replication are other main causes of treatment failure.

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The Application of Arsenic Trioxide in Ameliorating ABT-737 Target Therapy on Uterine Cervical Cancer Cells through Unique Pathways in Cell Death

Cited by 14 publications

References 48 publications

Suppression of PI3K/Akt/mTOR/c-Myc/mtp53 Positive Feedback Loop Induces Cell Cycle Arrest by Dual PI3K/mTOR Inhibitor PQR309 in Endometrial Cancer Cell Lines

Suppression of PI3K/Akt/mTOR/c-Myc/mtp53 Positive Feedback Loop Induces Cell Cycle Arrest by Dual PI3K/mTOR Inhibitor PQR309 in Endometrial Cancer Cell Lines

CLEFMA induces intrinsic and extrinsic apoptotic pathways through ERK1/2 and p38 signalling in uterine cervical cancer cells

A recent development of new therapeutic agents and novel drug targets for cancer treatment

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