Hedgehog Signaling in Pancreatic Fibrosis and Cancer

Bai, Yongyu; Bai, Yongheng; Dong, Jiaojiao; Li, Qiang; Jin, Yuepeng; Chen, Bicheng; Zhou, Mengtao

doi:10.1097/md.0000000000002996

Cited by 41 publications

(33 citation statements)

References 149 publications

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“…Hedgehog signaling has an important relationship to tumorigenesis [196,197]. Overexpression of Hh and Gli1 associates with the start of pancreatic ductal neoplasia [198,199].…”

Section: Crosstalk With Other Pathwaysmentioning

confidence: 99%

“…In pancreatic cancer was reported a ligand-dependent activation of Hedgehog signaling, while in other cancers, genomic mutations were reported. The Sonic Hedgehog (Shh) overexpression seems to trigger the onset of pancreatic cancer [196]. Shh, along with that of Smo and Gli, is present on stromal-derived PSCs.…”

Section: Crosstalk With Other Pathwaysmentioning

confidence: 99%

“…The Hedgehog signal ligands released by cancer cells induced the secretion by PCDs of cancer cells stimulating factors [202]. Hedgehog signaling has an important relationship to tumorigenesis [196,197]. Overexpression of Hh and Gli1 associates with the start of pancreatic ductal neoplasia [198,199].…”

Section: Crosstalk With Other Pathwaysmentioning

confidence: 99%

See 2 more Smart Citations

CD36 and CD97 in Pancreatic Cancer versus Other Malignancies

Tănase

Gheorghișan-Gălățeanu

Popescu

et al. 2020

IJMS

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Starting from the recent identification of CD36 and CD97 as a novel marker combination of fibroblast quiescence in lung during fibrosis, we aimed to survey the literature in search for facts about the separate (or concomitant) expression of clusters of differentiation CD36 and CD97 in either tumor- or pancreatic-cancer-associated cells. Here, we provide an account of the current knowledge on the diversity of the cellular functions of CD36 and CD97 and explore their potential (common) contributions to key cellular events in oncogenesis or metastasis development. Emphasis is placed on quiescence as an underexplored mechanism and/or potential target in therapy. Furthermore, we discuss intricate signaling mechanisms and networks involving CD36 and CD97 that may regulate different subpopulations of tumor-associated cells, such as cancer-associated fibroblasts, adipocyte-associated fibroblasts, tumor-associated macrophages, or neutrophils, during aggressive pancreatic cancer. The coexistence of quiescence and activated states in cancer-associated cell subtypes during pancreatic cancer should be better documented, in different histological forms. Remodeling of the local microenvironment may also change the balance between growth and dormant state. Taking advantage of the reported data in different other tissue types, we explore the possibility to induce quiescence (similar to that observed in normal cells), as a therapeutic option to delay the currently observed clinical outcome.

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“…Hedgehog signaling has an important relationship to tumorigenesis [196,197]. Overexpression of Hh and Gli1 associates with the start of pancreatic ductal neoplasia [198,199].…”

Section: Crosstalk With Other Pathwaysmentioning

confidence: 99%

Section: Crosstalk With Other Pathwaysmentioning

confidence: 99%

See 1 more Smart Citation

CD36 and CD97 in Pancreatic Cancer versus Other Malignancies

Tănase

Gheorghișan-Gălățeanu

Popescu

et al. 2020

IJMS

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“…The present study focused on the association between HO-1 and SHH in PC. As reported previously, SHH regulates pancreatic fibrosis and cancer cell proliferation and differentiation (22,23). Gem is one of the most important chemotherapeutic agents used in the treatment of the majority of patients with PC (13,24).…”

Section: Discussionmentioning

confidence: 68%

The inhibition of heme oxygenase-1 enhances the chemosensitivity and suppresses the proliferation of pancreatic cancer cells through the SHH signaling pathway

Han

Jiang

et al. 2018

Int J Oncol

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Pancreatic cancer (PC) is a type of cancer associated with a high fatality rate due to a poor prognosis and resistance to treatment. Heme oxygenase-1 (HO-1) is significantly overexpressed in a number of types of cancer and seems to play an important role in cancer progression. In this study, we examined the potential effects of HO-1 on PC cell proliferation and sensivity to gemcitabine (Gem). Furthermore, the role of the sonic hedgehog (SHH) signaling pathway in the regulatory effects of HO-1 on PC progression were examined. For this purpose, the expression of HO-1 was examined in cultured PC cells by real-time PCR, western blot analysis and immunofluorescence. Transfection with small interfering RNA against HO-1 or an overexpression plasmid were used to regulate the expression of HO-1 in the MIA PaCa-2 and PANC-1 cell lines. Cell proliferation was examined by MTT assays in response to the different treatments. The results revealed that HO-1 expression differed significantly in the different PC cells. The overexpression of HO-1 induced PC cell proliferation and the inhibition of HO-1 decreased the cell proliferative ability. Furthermore, HO-1 activated the SHH signaling pathway in the PC cells. In addition, the SHH signaling pathway was found to play a role in HO-1-induced PC cell proliferation. The inhibition of HO-1 enhanced the responsiveness of PC cells to Gem and Gem was found to regulate the expression of HO-1 and the activation of the SHH pathway. On the whole, our findings indicate that HO-1 overexpression in PC cells may be responsible for the increased cell proliferation and the resistance to anticancer therapy. Furthermore, the SHH signaling pathway, the activation of which was initiated by HO-1, may be one of the endogenous mechanisms in this process. Our data shed light into the association between HO-1 and SHH in PC cells, and may aid in the development of novel therapeutic targets for the treatment of patients with PC.

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“…The list of top ten deregulated miRNAs identified in these studies is shown in Table 1. Moreover, identification of pancreatitis associated genes as targets of deregulated miRNAs and their involvement in relevant pathways leading to pancreatitis is further supported by studies which have independently identified deregulated genes as important factors in epithelial-stromal signaling in pancreatic desmoplasia (Binkley et al, 2004) and pancreatitis associated pancreatic fibrosis (Bai et al, 2016). In addition to these studies, there are few other studies where different groups have compared the expression of individual miRNAs to evaluate their functional role.…”

Section: Role Of Mirnas In Chronic Pancreatitismentioning

confidence: 99%

Role of Noncoding RNAs in Chronic Pancreatitis

Chhatriya

Sarkar

Goswami

2018

Proceedings of the Indian National Science Academy

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Chronic pancreatitis (CP) is a progressive inflammatory disease of pancreas, resulting in irreversible damage of exocrine and endocrine function of the organ. Tissue fibrosis is a characteristic feature of CP, where the pancreatic stellate cells have been thought to play a very crucial role. Patients with chronic pancreatitis have also been reported to be more susceptible to pancreatic cancer as compared to any healthy individual. Considering the public health importance of the disease, efforts are underway to comprehend the alterations in gene expression pattern during the development and progression of the disease. Non-coding RNAs (ncRNAs) do not code for any proteins, but they are the key players in modulating the expression of large number of protein coding genes, consequently maintaining their normal function as well as adversely affecting the gene expression leading to disease pathophysiology. In recent years, studies on ncRNAs have gained much importance with the discovery of more and more types of ncRNAs and their involvement in almost every disease. Same is true for chronic pancreatitis as well, and the ncRNAs have been implicated to have important regulatory role in the biology of this disease. Furthermore, they have also been shown to have the ability to be used as diagnostic and prognostic biomarkers of this disease. This review highlights the major findings in the field of ncRNAs (especially microRNAs and long noncoding RNAs) with respect to chronic pancreatitis in humans.

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Hedgehog Signaling in Pancreatic Fibrosis and Cancer

Cited by 41 publications

References 149 publications

CD36 and CD97 in Pancreatic Cancer versus Other Malignancies

CD36 and CD97 in Pancreatic Cancer versus Other Malignancies

The inhibition of heme oxygenase-1 enhances the chemosensitivity and suppresses the proliferation of pancreatic cancer cells through the SHH signaling pathway

Role of Noncoding RNAs in Chronic Pancreatitis

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