Advances in CRC Prevention: Screening and Surveillance

Dekker, Evelien; Rex, Douglas K.

doi:10.1053/j.gastro.2018.01.069

Cited by 122 publications

(104 citation statements)

References 157 publications

(153 reference statements)

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“…The incidence has stabilized or is declining in the US and some other developed countries, but the incidence and mortality are increasing in some developing countries, especially China and Spain 2,3 . Although great progress has been achieved in surgical techniques and treatment for CRC, the 5-year relative survival rate of CRC patients has not changed significantly in the past decades 4,5 . Therefore, there is an urgent need to better understand the molecular mechanisms that govern the oncogenesis and progression of CRC.…”

mentioning

confidence: 99%

Fasting inhibits aerobic glycolysis and proliferation in colorectal cancer via the Fdft1-mediated AKT/mTOR/HIF1α pathway suppression

et al. 2020

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Evidence suggests that fasting exerts extensive antitumor effects in various cancers, including colorectal cancer (CRC). However, the mechanism behind this response is unclear. We investigate the effect of fasting on glucose metabolism and malignancy in CRC. We find that fasting upregulates the expression of a cholesterogenic gene, Farnesyl-Diphosphate Farnesyltransferase 1 (FDFT1), during the inhibition of CRC cell aerobic glycolysis and proliferation. In addition, the downregulation of FDFT1 is correlated with malignant progression and poor prognosis in CRC. Moreover, FDFT1 acts as a critical tumor suppressor in CRC. Mechanistically, FDFT1 performs its tumor-inhibitory function by negatively regulating AKT/mTOR/ HIF1α signaling. Furthermore, mTOR inhibitor can synergize with fasting in inhibiting the proliferation of CRC. These results indicate that FDFT1 is a key downstream target of the fasting response and may be involved in CRC cell glucose metabolism. Our results suggest therapeutic implications in CRC and potential crosstalk between a cholesterogenic gene and glycolysis.

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confidence: 99%

Fasting inhibits aerobic glycolysis and proliferation in colorectal cancer via the Fdft1-mediated AKT/mTOR/HIF1α pathway suppression

et al. 2020

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“…Remarkably, up to 65% of patients with stage IV CRC have relapsed disease after treatment with curative intent, while on 30% of patients with stage I-III CRC experience relapse after similar treatment [3]. Although modern curative treatments have already greatly improved the overall survival (OS) and disease-free survival (DFS) of patients with CRC in recent years, the success of these treatment strategies is generally based on early detection of primary and recurrent CRC [4,5]. Therefore, further exploration of the molecular mechanism underlying CRC recurrence and metastasis and identi cation of candidate biomarkers of these processes are urgently needed and important for improving the CRC survival rate.…”

Section: Introductionmentioning

confidence: 99%

Downregulation of PLK4 Expression Induces Cellular Dormancy in Colorectal Cancer via Mesenchymal-to-epithelial Transition

Tian¹,

Liu²,

Zhou³

et al. 2020

Preprint

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Background: Reactivation of dormant tumor cells is a critical step in the recurrence of many cancers, including colorectal cancer (CRC). Polo-like kinases 4 (PLK4), a central regulator of the cell cycle and proliferation, is a validated oncogene in tumorigenesis. However, the roles of PLK4 in tumor cell dormancy and reactivation still need to be further explored.Methods: The expression level of PLK4 was determined by immunohistochemical staining, Western blotting (WB) and quantitative real-time PCR (qRT-PCR). PLK4-dependent clinicopathological risk factors and the prognosis of CRC were characterized with 122 clinical samples. The roles of PLK4 in tumor cell dormancy, cell cycle progression, proliferation and invasion were determined by molecular and cell biology methods in vitro and in vivo.Results: The expression of PLK4 was dramatically increased in CRCs and positively correlated with aggressive tumor behavior and clinicopathological risk factors. Downregulation of PLK4 expression contributed to restoring phenotypically aggressive tumor cells to a quiescent state, and this transformation was likely regulated by mesenchymal-to-epithelial transformation (MET) progression in vitro and in vivo.Conclusions: This study elucidates the mechanisms involving PLK4 depletion in the induction and maintenance of CRC dormancy, which are very important in terms of both clinical significance and application value.

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“…Colorectal cancer (CRC) is one of the most common malignant neoplasms with poor prognosis and high frequency of recurrence [1], accounting for 600,000 mortalities per year worldwide. Tumor recurrence and metastasis to distant organs are the main factors for the high mortality and low survival rates [2].…”

Section: Introductionmentioning

confidence: 99%

RNAi mediated silencing of Nanog expression suppresses the growth of human colorectal cancer stem cells

Zhang

Zhao

Yang

et al. 2020

Preprint

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Background: Colorectal cancer (CRC) is the third most common cancer in the world known for its poor recurrence-free prognosis. Previous studies have shown that it is closely linked with cancer stem cells (CSCs), which have self-renewal potential and the capacity to differentiate into diverse populations. Nanog is an important transcription factor that functions to maintain the self-renewal and proliferation of embryonic stem cells; however, many recent studies have shown that Nanog is also highly expressed in many cancer stem cells. Methods: To investigate whether Nanog plays a crucial role in maintaining the stemness of colorectal CSCs (CCSCs), RNA interference was used to downregulate Nanog expression in the CRC stem cell line, EpCAM + CD44 + HCT-116. We examined the anti-tumor function of Nanog in vitro and in vivo, using small interfering RNA. Results: Our results revealed that the Nanog mRNA expression level in CCSCs was higher than that in HCT-116 cells. We found that the depletion of Nanog inhibited proliferation and promoted apoptosis in EpCAM + CD44 + HCT-116 cells. In addition, the invasive ability of EpCAM + CD44 + HCT-116 cells was markedly restricted when Nanog was silenced by small interfering RNA. Furthermore, we found that the silencing of Nanog decreased tumor size and weight and improved the survival rate of tumor-bearing mice. Conclusions: In conclusion, these findings collectively demonstrate that Nanog, which is highly expressed in CRC stem cells, is a key factor in the development of tumor growth, and it may serve as a potential marker of prognosis and a novel and effective therapeutic target for the treatment of CRC.

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Advances in CRC Prevention: Screening and Surveillance

Cited by 122 publications

References 157 publications

Fasting inhibits aerobic glycolysis and proliferation in colorectal cancer via the Fdft1-mediated AKT/mTOR/HIF1α pathway suppression

Fasting inhibits aerobic glycolysis and proliferation in colorectal cancer via the Fdft1-mediated AKT/mTOR/HIF1α pathway suppression

Downregulation of PLK4 Expression Induces Cellular Dormancy in Colorectal Cancer via Mesenchymal-to-epithelial Transition

RNAi mediated silencing of Nanog expression suppresses the growth of human colorectal cancer stem cells

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