Peptidergic Systems and Cancer: Focus on Tachykinin and Calcitonin/Calcitonin Gene-Related Peptide Families

Sánchez, Manuel Lisardo; Rodríguez, Fernando Mateos; Coveñas, Rafael

doi:10.3390/cancers15061694

Cited by 10 publications

(11 citation statements)

References 359 publications

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“…Our future studies will address these knowledge gaps. The findings of decreased endothelial cells in the lungs of LPS-exposed Adm-haplodeficient (Adm +/− ) mice reconfirm the proangiogenic effects of Adm [43][44][45]47,[105][106][107][108] and the importance of endothelial cell health in mitigating BPD [12,13,70]. Type II pneumocytes play a vital role in BPD pathogenesis.…”

Section: Discussionmentioning

confidence: 82%

Leveraging Integrated RNA Sequencing to Decipher Adrenomedullin’s Protective Mechanisms in Experimental Bronchopulmonary Dysplasia

Palit,

Shrestha,

Thapa

et al. 2024

Genes

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Bronchopulmonary dysplasia (BPD) is a chronic lung disease commonly affecting premature infants, with limited therapeutic options and increased long-term consequences. Adrenomedullin (Adm), a proangiogenic peptide hormone, has been found to protect rodents against experimental BPD. This study aims to elucidate the molecular and cellular mechanisms through which Adm influences BPD pathogenesis using a lipopolysaccharide (LPS)-induced model of experimental BPD in mice. Bulk RNA sequencing of Adm-sufficient (wild-type or Adm+/+) and Adm-haplodeficient (Adm+/−) mice lungs, integrated with single-cell RNA sequencing data, revealed distinct gene expression patterns and cell type alterations associated with Adm deficiency and LPS exposure. Notably, computational integration with cell atlas data revealed that Adm-haplodeficient mouse lungs exhibited gene expression signatures characteristic of increased inflammation, natural killer (NK) cell frequency, and decreased endothelial cell and type II pneumocyte frequency. Furthermore, in silico human BPD patient data analysis supported our cell type frequency finding, highlighting elevated NK cells in BPD infants. These results underscore the protective role of Adm in experimental BPD and emphasize that it is a potential therapeutic target for BPD infants with an inflammatory phenotype.

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Section: Discussionmentioning

confidence: 82%

Leveraging Integrated RNA Sequencing to Decipher Adrenomedullin’s Protective Mechanisms in Experimental Bronchopulmonary Dysplasia

Palit,

Shrestha,

Thapa

et al. 2024

Genes

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“…Numerous studies have indicated increased serum CGRP levels in breast, lung, thyroid, and prostate cancers [14,[35][36][37][38][39]. However, the data in the literature related to the tissue expression of CGRP in the normal and tumor colon are practically non-existent.…”

Section: Discussionmentioning

confidence: 99%

Expression of Calcitonin Gene-Related Peptide and Calcitonin Receptor-like Receptor in Colorectal Adenocarcinoma

Șerban,

Stepan,

Florescu

et al. 2024

IJMS

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Colorectal cancer is one of the most widespread types of cancer that still causes many deaths worldwide. The development of new diagnostic and prognostic markers, as well as new therapeutic methods, is necessary. The calcitonin gene-related peptide (CGRP) neuropeptide alongside its receptor calcitonin receptor-like receptor (CRLR) could represent future biomarkers and a potential therapeutic target. Increased levels of CGRP have been demonstrated in thyroid, prostate, lung, and breast cancers and may also have a role in colorectal cancer. At the tumor level, it acts through different mechanisms, such as the angiogenesis, migration, and proliferation of tumor cells. The aim of this study was to measure the level of CGRP in colorectal cancer patients’ serum by enzyme-linked immunosorbent assay (ELISA) and determine the level of CGRP and CRLR at the tumor level after histopathological (HP) and immunohistochemical (IHC) analysis, and then to correlate them with the TNM stage and with different tumoral characteristics. A total of 54 patients with newly diagnosed colorectal adenocarcinoma were evaluated. We showed that serum levels of CGRP, as well as CGRP and CRLR tumor level expression, correlate with the TNM stage, with local tumor extension, the presence of lymph node metastasis, and distant metastasis, and also with the tumor differentiation degree. CGRP is present in colorectal cancer from the incipient TNM stage, with levels increasing with the stage, and can be used as a diagnostic and prognostic marker and may also represent a potentially new therapeutic target.

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“…Cisplatin [83] and oxaliplatin also stimulate TRPV1 expression [84] (along with TRPA1 [84] and TRPM8 [85]) in sensory afferents. TRPV1-expressing nerve endings release calcitonin gene-related peptide (CGRP) that, in turn, can stimulate cancer growth [73][74][75]. In a murine cancer model (Lewis carcinoma inoculated into the paw), tumor growth was attenuated in both TRPV1-null and αCGRP-null mice compared to in wild-type littermates [76].…”

Section: Trpv1 In Cancer Pain: Molecular Mechanismsmentioning

confidence: 99%

Targeting TRPV1 for Cancer Pain Relief: Can It Work?

Szallasi

2024

Cancers

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Chronic intractable pain affects a large proportion of cancer patients, especially those with metastatic bone disease. Blocking sensory afferents for cancer pain relief represents an attractive alternative to opioids and other drugs acting in the CNS in that sensory nerve blockers are not addictive and do not affect the mental state of the patient. A distinct subpopulation of sensory afferents expresses the capsaicin receptor TRPV1. Intrathecal resiniferatoxin, an ultrapotent capsaicin analog, ablates TRPV1-expressing nerve endings exposed to the cerebrospinal fluid, resulting in permanent analgesia in women with cervical cancer metastasis to the pelvic bone. High-dose capsaicin patches are effective pain killers in patients with chemotherapy-induced peripheral neuropathic pain. However, large gaps remain in our knowledge since the mechanisms by which cancer activates TRPV1 are essentially unknown. Most important, it is not clear whether or not sensory denervation mediated by TRPV1 agonists affects cancer progression. In a murine model of breast cancer, capsaicin desensitization was reported to accelerate progression. By contrast, desensitization mediated by resiniferatoxin was found to block melanoma growth. These observations imply that TRPV1 blockade for pain relief may be indicated for some cancers and contraindicated for others. In this review, we explore the current state of this field and compare the analgesic potential of TRPV1 antagonism and sensory afferent desensitization in cancer patients.

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Peptidergic Systems and Cancer: Focus on Tachykinin and Calcitonin/Calcitonin Gene-Related Peptide Families

Cited by 10 publications

References 359 publications

Leveraging Integrated RNA Sequencing to Decipher Adrenomedullin’s Protective Mechanisms in Experimental Bronchopulmonary Dysplasia

Leveraging Integrated RNA Sequencing to Decipher Adrenomedullin’s Protective Mechanisms in Experimental Bronchopulmonary Dysplasia

Expression of Calcitonin Gene-Related Peptide and Calcitonin Receptor-like Receptor in Colorectal Adenocarcinoma

Targeting TRPV1 for Cancer Pain Relief: Can It Work?

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