Autophagy and cancer treatment: four functional forms of autophagy and their therapeutic applications

Bai, Zhaoshi; Peng, Yaling; Ye, Xinyue; Liu, Zhixian; Li, Yupeng; Ma, Lingman

doi:10.1631/jzus.b2100804

Cited by 26 publications

(18 citation statements)

References 89 publications

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“…In cervical cancer cells, T antigen promoted proliferation and inhibited apoptosis by downregulating p21, p27, p53, and AIF, upregulating XIAP, or activating the PI3K/Akt/mTOR and PI3K/Akt/NF-κB/survivin pathways. Pyroptosis is a recently discovered form of in ammatory programmed necrosis characterized by gasdermin D-dependent cell death while autophagy is characterized by LC-3B activation [40,41]. ZEB1 promotes epithelialmesenchymal transition (EMT) with low expression of E-cadherin and overexpression of N-cadherin and vimentin [42].…”

Section: Discussionmentioning

confidence: 99%

The oncogenic roles of JC polyomavirus T antigen in cervical cancer

Xue

Zheng

et al. 2022

Preprint

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BackgroundAccording to pathological and transgenic data, there is a close link between JC polyomavirus (JCPyV) T antigen and various epithelial cancers. The aim of this study was to explore the role of T antigen in cervical tumorigenesis.MethodsThe phenotypes were observed in T antigen-overexpressing HeLa cells by Cell Counting Kit-8 assay, Annexin V staining, Transwell assay, and a xenograft model. Phenotype-related and T antigen partner proteins were screened by western blot. Nested, real-time, and in situ PCR were used to detect T antigen in cervical cancer.ResultsOverexpression of T antigen promoted the proliferation, anti-apoptosis, anti-pyroptosis, chemoresistance, migration, invasion, and epithelial-mesenchymal transition of HeLa cells. All mutants impaired the positively regulated effects of T antigen on proliferation. According to a general PCR, the positive rate of T antigen was higher in cervical cancer than in adjacent cervical intraepithelial neoplasia (CIN) and normal tissues (p < 0.05), in line with the JCPyV copy number (p < 0.05). T antigen-positive cells were detectable in the nuclei of cervical cancer, CIN, and squamous cells by in situ PCR. Strong nuclear immunoreactivity against T antigen was observed in cervical cancers, but not in CIN or normal squamous epithelium.ConclusionsJCPyV T antigen may insert into the genome of cervical squamous epithelial cells and encode T antigen for its oncogenesis. T antigen participates in the aggressive progression of these cells by promoting proliferation, anti-apoptosis, anti-pyroptosis, migration, invasion, epithelial-mesenchymal transition, and chemoresistance.

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Section: Discussionmentioning

confidence: 99%

The oncogenic roles of JC polyomavirus T antigen in cervical cancer

Xue

Zheng

et al. 2022

Preprint

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“…Autophagy is a highly programmed process of lysosome-mediated degradation, which is a conserved cellular defensive mechanism against various stress stimuli such as oxidation, nutrient deprivation, ER stress, and DNA damage [131,132]. The mTOR kinase plays a central role in the regulation of autophagy induction, as its activation by AKT and MAPK inhibit autophagy induction while its inhibition by AMPK and p53 promotes autophagy induction [131][132][133]. The activation of autophagy signaling begins with the inhibition of mTOR kinase and activation of ULK kinase, which subsequently complexes with and activates ATG13 and FIP200.…”

Section: Radiation Activates the Autophagy Signaling Pathway That Lea...mentioning

confidence: 99%

“…Generally, the function of autophagy is thought to promote cell survival through maintaining energetic homeostasis. However, autophagy can also induce cell death to eliminate the seriously damaged cells [131,132,134]. It has been known that radiation-produced ROS/RNS not only causes oxidative stress and impedes mitochondrial function in cells but also induces DSB/SSB DNA damage, all of which can trigger autophagic response leading to cell death or survival.…”

Section: Radiation Activates the Autophagy Signaling Pathway That Lea...mentioning

confidence: 99%

Cell Signaling Pathways That Promote Radioresistance of Cancer Cells

2022

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Radiation therapy (RT) is a standard treatment for solid tumors and about 50% of patients with cancer, including pediatric cancer, receive RT. While RT has significantly improved the overall survival and quality of life of cancer patients, its efficacy has still been markedly limited by radioresistance in a significant number of cancer patients (intrinsic or acquired), resulting in failure of the RT control of the disease. Radiation eradicates cancer cells mainly by causing DNA damage. However, radiation also concomitantly activates multiple prosurvival signaling pathways, which include those mediated by ATM, ATR, AKT, ERK, and NF-κB that promote DNA damage checkpoint activation/DNA repair, autophagy induction, and/or inhibition of apoptosis. Furthermore, emerging data support the role of YAP signaling in promoting the intrinsic radioresistance of cancer cells, which occurs through its activation of the transcription of many essential genes that support cell survival, DNA repair, proliferation, and the stemness of cancer stem cells. Together, these signaling pathways protect cancer cells by reducing the magnitude of radiation-induced cytotoxicity and promoting radioresistance. Thus, targeting these prosurvival signaling pathways could potentially improve the radiosensitivity of cancer cells. In this review, we summarize the contribution of these pathways to the radioresistance of cancer cells.

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“…Autophagy also known as type II programmed cell death plays a critical role in cancer. Autophagy has an active tumor-suppressive or tumor-stimulating function in various process and stages of cancer development (Bai et al 2022). In the early stage of cancer, autophagy acts as a survival pathway and quality-control mechanism inhibits tumor initiation and suppresses cancer progression.…”

Section: Effect Of Sa On Autophagymentioning

confidence: 99%

Mechanisms involved in the anticancer effects of sinapic acid

Anandakumar

Kalappan

2022

Bull Natl Res Cent

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Background Cancer refers to a group of diseases characterized by the development of abnormal cells that divide uncontrollably and have the ability to infiltrate and destroy normal body tissue. Worldwide, it is the second most leading cause of death. Dietary intake of bioactive compounds from plant sources has been documented for their protective effect against different types of human ailments including cancer. Main body Sinapic acid (3,5-dimethoxy-4-hydroxycinnamic acid) (SA) is a promising phytochemical, available in oil seeds, berries, spices, vegetables and cereals. SA has been well documented for its antibacterial, anti-peroxidative, anti-hyperglycemic, anticancer, hepatoprotective, reno-protective, anti-inflammatory, neuroprotective, immunomodulatory and anticancer effects. Nevertheless, the anticancer activity of SA has remained a challenge with regard to understanding its mechanism in health and diseases. Short conclusion This review is an effort to summarize the updated literature available about the mechanisms involved in the anticancer effects of SA in order to recommend this compound for further future investigations.

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Autophagy and cancer treatment: four functional forms of autophagy and their therapeutic applications

Cited by 26 publications

References 89 publications

The oncogenic roles of JC polyomavirus T antigen in cervical cancer

The oncogenic roles of JC polyomavirus T antigen in cervical cancer

Cell Signaling Pathways That Promote Radioresistance of Cancer Cells

Mechanisms involved in the anticancer effects of sinapic acid

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