Publications by authors named "Ana Karina Aranda-Rivera"

6 Publications

  • Page 1 of 1

Lipid metabolism and oxidative stress in HPV-related cancers.

Free Radic Biol Med 2021 Jun 12;172:226-236. Epub 2021 Jun 12.

IHuman Institute, ShanghaiTech University, China; Laboratorio F-206, Departamento de Biología, Facultad de Química, Universidad Nacional Autónoma de México, 04510, Ciudad de México, Mexico. Electronic address:

High-risk human papillomavirus (HR-HPVs) are associated with the development of cervical, anus, vagina, vulva, penis, and oropharynx cancer. HR-HPVs target and modify the function of different cell biomolecules such as glucose, amino acids, lipids, among others. The latter induce cell proliferation, cell death evasion, and genomic instability resulting in cell transformation. Moreover, lipids are essential biomolecules in HR-HPVs infection and cell vesicular trafficking. They are also critical in producing cellular energy, the epithelial-mesenchymal transition (EMT) process, and therapy resistance of HPV-related cancers. HPV proteins induce oxidative stress (OS), which in turn promotes lipid peroxidation and cell damage, resulting in cell death such as apoptosis, autophagy, and ferroptosis. HR-HPV-related cancer cells cope with OS and lipid peroxidation, preventing cell death; however, these cells are sensitized by OS, which could be used as a target for redox therapies to induce their elimination. This review focuses on the role of lipids in HR-HPV infection and HPV-related cancer development, maintenance, resistance to therapy, and the possible treatments associated with lipids. Furthermore, we emphasize the significant role of OS in lipid peroxidation to induce cell death through apoptosis, autophagy, and ferroptosis to eliminate HPV-related cancers.
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http://dx.doi.org/10.1016/j.freeradbiomed.2021.06.009DOI Listing
June 2021

Redox signaling pathways in unilateral ureteral obstruction (UUO)-induced renal fibrosis.

Free Radic Biol Med 2021 May 30;172:65-81. Epub 2021 May 30.

Laboratorio F-315, Departamento de Biología, Facultad de Química, Universidad Nacional Autónoma de México, 04510, Ciudad de México, Mexico. Electronic address:

Unilateral ureteral obstruction (UUO) is an experimental rodent model that mimics renal fibrosis associated with obstructive nephropathy in an accelerated manner. After UUO, the activation of the renin-angiotensin system (RAS), nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs) and mitochondrial dysfunction lead to reactive oxygen species (ROS) overproduction in the kidney. ROS are secondary messengers able to induce post-translational modifications (PTMs) in redox-sensitive proteins, which activate or deactivate signaling pathways. Therefore, in UUO, it has been proposed that ROS overproduction causes changes in said pathways promoting inflammation, oxidative stress, and apoptosis that contribute to fibrosis development. Furthermore, mitochondrial metabolism impairment has been associated with UUO, contributing to renal damage in this model. Although ROS production and oxidative stress have been studied in UUO, the development of renal fibrosis associated with redox signaling pathways has not been addressed. This review focuses on the current information about the activation and deactivation of signaling pathways sensitive to a redox state and their effect on mitochondrial metabolism in the fibrosis development in the UUO model.
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http://dx.doi.org/10.1016/j.freeradbiomed.2021.05.034DOI Listing
May 2021

Redox-sensitive signalling pathways regulated by human papillomavirus in HPV-related cancers.

Rev Med Virol 2021 Mar 11:e2230. Epub 2021 Mar 11.

Laboratorio F-315, Departamento de Biología, Facultad de Química, Universidad Nacional Autónoma de México, México City, México.

High-risk human papillomavirus (HR-HPV) chronic infection is associated with the induction of different HPV-related cancers, such as cervical, anus, vaginal, vulva, penis and oropharynx. HPV-related cancers have been related to oxidative stress (OS), where OS has a significant role in cancer development and maintenance. Surgical resection is the treatment of choice for localised HPV-related cancers; however, these malignancies commonly progress to metastasis. In advanced stages, systemic therapies are the best option against HPV-related cancers. These therapies include cytokine therapy or a combination of tyrosine kinase inhibitors with immunotherapies. Nevertheless, these strategies are still insufficient. Cell redox-sensitive signalling pathways have been poorly studied, although they have been associated with the development and maintenance of HPV-related cancers. In this review, we analyse the known alterations of the following redox-sensitive molecules and signalling pathways by HR-HPV in HPV-related cancers: MAPKs, Akt/TSC2/mTORC1, Wnt/β-Cat, NFkB/IkB/NOX2, HIF/VHL/VEGF and mitochondrial signalling pathways as potential targets for redox therapy.
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http://dx.doi.org/10.1002/rmv.2230DOI Listing
March 2021

Regulation of autophagy by high- and low-risk human papillomaviruses.

Rev Med Virol 2021 Mar 17;31(2):e2169. Epub 2020 Sep 17.

Laboratorio 315, Departamento de Biología, Facultad de Química, Universidad Nacional Autónoma de México, Mexico City, México.

While high-risk human papillomavirus (HR-HPV) infection is related to the development of cervical, vulvar, anal, penile and oropharyngeal cancer, low-risk human papillomavirus (LR-HPV) infection is implicated in about 90% of genital warts, which rarely progress to cancer. The carcinogenic role of HR-HPV is due to the overexpression of HPV E5, E6 and E7 oncoproteins which target and modify cellular proteins implicated in cell proliferation, apoptosis and immortalization. LR-HPV proteins also target and modify some of these processes; however, their oncogenic potential is lower than that of HR-HPV. HR-HPVs have substantial differences with LR-HPVs such as viral integration into the cell genome, induction of p53 and retinoblastoma protein degradation, alternative splicing in HR-HPV E6-E7 open reading frames, among others. In addition, LR-HPV can activate the autophagy process in infected cells while HR-HPV infection deactivates it. However, in cancer HR-HPV might reactivate autophagy in advance stages. Autophagy is a catabolic process that maintains cell homoeostasis by lysosomal degradation and recycling of damaged macromolecules and organelles; nevertheless, depending upon cellular context autophagy may also induce cell death. Therefore, autophagy can contribute either as a promotor or as a suppressor of tumours. In this review, we focus on the role of HR-HPV and LR-HPV in autophagy during viral infection and cancer development. Additionally, we review key regulatory molecules such as microRNAs in HPV present during autophagy, and we emphasize the potential use of cancer treatments associated with autophagy in HPV-related cancers.
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http://dx.doi.org/10.1002/rmv.2169DOI Listing
March 2021

Human Papillomavirus-related Cancers and Mitochondria.

Virus Res 2020 09 20;286:198016. Epub 2020 May 20.

Faculty of Chemistry, Biology Department, Laboratories F-315, National Autonomous University of Mexico, CDMX, 04510, Mexico. Electronic address:

Although it has been established that persistent infection with high risk human papillomavirus (HR-HPV) is the main cause in the development of cervical cancer, the HR-HPV infection is also related with the cause of a significant fraction of other human malignancies from the mucosal squamous epithelial such as anus, vagina, vulva, penis and oropharynx. HR-HPV infection induces cell proliferation, cell death evasion and genomic instability resulting in cell transformation, due to HPV proteins, which target and modify the function of differents cell molecules and organelles, such as mitochondria. Mitochondria are essential in the production of the cellular energy by oxidative phosphorylation (OXPHOS), in the metabolism of nucleotides, aminoacids (aa), and fatty acids, even in the regulation of cell death processes such as apoptosis or mitophagy. Thus, mitochondria have a significant role in the HPV-related cancer development. This review focuses on the role of HPV and mitochondria in HPV-related cancer development, and treatments associated to mitochondrial apoptosis.
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http://dx.doi.org/10.1016/j.virusres.2020.198016DOI Listing
September 2020

E6 Oncoproteins from High-Risk Human Papillomavirus Induce Mitochondrial Metabolism in a Head and Neck Squamous Cell Carcinoma Model.

Biomolecules 2019 08 8;9(8). Epub 2019 Aug 8.

Unidad de Investigación Biomédica en Cáncer, Instituto Nacional de Cancerología, México/Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México. San Fernando No. 22, Col. Sección XVI, Tlalpan, Ciudad de México 14080, Mexico.

Head and neck squamous cell carcinoma (HNSCC) cells that are positive for human papillomavirus (HPV+) favor mitochondrial metabolism rather than glucose metabolism. However, the involvement of mitochondrial metabolism in HNSCC HPV+ cells is still unknown. The aim of this work was to evaluate the role of E6 oncoproteins from HPV16 and HPV18 in the mitochondrial metabolism in an HNSCC model. We found that E6 from both viral types abates the phosphorylation of protein kinase B-serine 473 (pAkt), which is associated with a shift in mitochondrial metabolism. E6 oncoproteins increased the levels of protein subunits of mitochondrial complexes (I to IV), as well as the ATP synthase and the protein levels of the voltage dependent anion channel (VDAC). Although E6 proteins increased the basal and leak respiration, the ATP-linked respiration was not affected, which resulted in mitochondrial decoupling. This increase in leak respiration was associated to the induction of oxidative stress (OS) in cells expressing E6, as it was observed by the fall in the glutathione/glutathione disulfide (GSH/GSSG) rate and the increase in reactive oxygen species (ROS), carbonylated proteins, and DNA damage. Taken together, our results suggest that E6 oncoproteins from HPV16 and HPV18 are inducers of mitochondrial metabolism.
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http://dx.doi.org/10.3390/biom9080351DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6722992PMC
August 2019
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