Corticotropin-Releasing Hormone Receptor Alters the Tumor Development and Growth in Apcmin/+ Mice and in a Chemically-Induced Model of Colon Cancer

Lee, Yunna; Elise, L.; Patel, Marisa; Kim, Gayoung; Howe, Cody; Pothoulakis, Charalabos; Kim, Yong‐Sung; Rhee, Sang Hoon

doi:10.3390/ijms22031043

Cited by 2 publications

(4 citation statements)

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“…And the results show that in WT (Crhr 109). These results are in concert with the report that CRF 2 deficiency worsens CRC in AOM/DSS model (56). However, opposite effect of CRF 2 is also reported, i.e.…”

Section: Peripheral Crh's Role In Colitisassociated Colon Cancersupporting

confidence: 90%

“…CRF 1 deficiency inhibits CRC in AOM/DSS model(56). Taken together, CRH/CRF 1 signaling promotes human colon cancer cell proliferation via NF-kB/IL-6/STAT3 and tumor angiogenesis via NF-kB/VEGF signaling pathway.…”

mentioning

confidence: 73%

“…Also, it is reported that CRH may induce intestinal hyperpermeability in human colon mucosa via mast cells (48). We and others have also reported the direct peripheral role of CRH/ UCNs & receptors in immunity/inflammation and cancers (42, [49][50][51][52][53][54], including colitis and colitis-associated colon cancer (CAC) (55)(56)(57)(58).…”

Section: Introductionmentioning

confidence: 99%

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Role of CRH in colitis and colitis-associated cancer: a combinative result of central and peripheral effects?

Zhu,

2024

Front. Endocrinol.

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Corticotropin-releasing factor family peptides (CRF peptides) comprise corticotropin releasing hormone (CRH), urocortin (UCN1), UCN2 and UCN3. CRH is first isolated in the brain and later with UCNs found in many peripheral cells/tissues including the colon. CRH and UCNs function via the two types of receptors, CRF1 and CRF2, with CRH mainly acting on CRF1, UCN1 on both CRF1 &CRF2 and UCN2-3 on CRF2. Compiling evidence shows that CRH participates in inflammation and cancers via both indirect central effects related to stress response and direct peripheral influence. CRH, as a stress-response mediator, plays a significant central role in promoting the development of colitis involving colon motility, immunity and gut flora, while a few anti-colitis results of central CRH are also reported. Moreover, CRH is found to directly influence the motility and immune/inflammatory cells in the colon. Likewise, CRH is believed to be greatly related to tumorigenesis of many kinds of cancers including colon cancer via the central action during chronic stress while the peripheral effects on colitis-associated-colon cancer (CAC) are also proved. We and others observe that CRH/CRF1 plays a significant peripheral role in the development of colitis and CAC in that CRF1 deficiency dramatically suppresses the colon inflammation and CAC. However, up to date, there still exist not many relevant experimental data on this topic, and there seems to be no absolute clearcut between the central and direct peripheral effects of CRH in colitis and colon cancer. Taken together, CRH, as a critical factor in stress and immunity, may participate in colitis and CAC as a centrally active molecule; meanwhile, CRH has direct peripheral effects regulating the development of colitis and CAC, both of which will be summarized in this review.

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Section: Peripheral Crh's Role In Colitisassociated Colon Cancersupporting

confidence: 90%

mentioning

confidence: 73%

Section: Introductionmentioning

confidence: 99%

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Role of CRH in colitis and colitis-associated cancer: a combinative result of central and peripheral effects?

Zhu,

2024

Front. Endocrinol.

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“…The effect of CRF is cancer-type specific: CRF binding to the CRF receptor can potentiate an anti-tumor response in endometrial cancer 45 and promote cancer progression in colon cancer 46 or breast cancer for instance 41 . Orexin receptors are expressed in gastric cancer (including esophageal cancer) and treatment with orexin has been shown to induce apoptosis in colorectal, neuroblastoma and pancreatic cancer cells 43 .…”

Section: Cansig Rediscovers Previously Investigated Signatures In Thr...mentioning

confidence: 99%

CanSig: discovery of shared transcriptional states across cancer patients from single-cell RNA sequencing data

Yates

Barkmann

Czyz

et al. 2022

Preprint

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Human tumors are highly heterogeneous in their cell composition; specifically, they exhibit heterogeneity in transcriptional states of malignant cells, as has been recently discovered through single-cell RNA sequencing (scRNA-seq). Distinct states of malignant cells have been linked to variability in tumorigenic properties and resistance to anti-cancer treatment. Despite the fact that scRNA-seq data contain all necessary information to uncover shared transcriptional states of malignant cells in tumors, jointly analyzing cells from multiple cancer patients comes with its set of challenges including batch correction and accounting for patient-specific genetic background driving differences between gene expression vectors. We propose CanSig, an easy-to-use approach designed to discover known and de novo shared signatures in cancer single cells. CanSig preprocesses, integrates and analyzes scRNA-seq data to provide new signatures of shared transcriptional states and links these states to known pathways. We show that CanSig successfully rediscovers ground truth pathways determining shared transcriptional states in two simulated and three experimental datasets; the latter spanning 135 patients and 72,000 cells. We then illustrate CanSig's investigative potential by discovering novel signatures in esophageal squamous cell carcinoma possibly linked to targeted patient treatment; we also point out a de novo signature in breast cancer predictive of patients' survival. In the cancer types studied, we juxtapose copy number variation with discovered shared transcriptional states and uncover a genetic component predisposing cancer cells to activation of specific transcriptional programs. In sum, CanSig, specifically developed to analyze shared transcriptional heterogeneity of malignant cells of different genetic backgrounds, can greatly facilitate the exploratory analysis of scRNA-seq cancer data and efficiently identify novel transcriptional signatures linked to known biological pathways.

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Corticotropin-Releasing Hormone Receptor Alters the Tumor Development and Growth in Apcmin/+ Mice and in a Chemically-Induced Model of Colon Cancer

Cited by 2 publications

References 44 publications

Role of CRH in colitis and colitis-associated cancer: a combinative result of central and peripheral effects?

Role of CRH in colitis and colitis-associated cancer: a combinative result of central and peripheral effects?

CanSig: discovery of shared transcriptional states across cancer patients from single-cell RNA sequencing data

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