Effect of As2O3 on colorectal CSCs stained with ALDH1 in primary cell culture in�vitro

Ning, Ke; Ning, Wenlong; Ning, Xiaoting; Wang, Xueyan; Zhou, Fei

doi:10.3892/ol.2018.9110

Cited by 3 publications

(4 citation statements)

References 18 publications

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“…HH signaling is also necessary for the growth of CRC xenografts, recurrence, and induction of EMT necessary for metastases [ 169 ]. In contrast, arsenic trioxide, an anti‐leukemic drug known to inhibit the HH signaling pathway by targeting GLI1 [ 170 ], increased CRC‐SCs from patient samples [ 171 ].…”

Section: Cell Signaling Pathwaysmentioning

confidence: 99%

“…Suppresses GSK-3β/Wnt/β-catenin signaling [118] 4-Acetyl-antroquinonol B Suppresses LGR5/Wnt/β-catenin and JAK-STAT signaling [104] Anti-DLL4 antibodies Suppresses Notch signaling [158] Atractylenolide I Suppresses Akt/mTOR signaling [225] Baicalin Suppresses TGF-β/Smad signaling [244] Buparlisib (BKM120) Suppresses PI3K/Akt/mTOR signaling by inhibition of PI3K [210] CBB1003 Suppresses β-catenin/TCF signaling [119] Cucurbitacins Suppresses Notch signaling by downregulation of the expression of ADAM9 [142] Curcumin Suppresses JAK/STAT signaling by inhibition of STAT3 [195] Cyclopamine Suppresses HH signaling by inhibition of SMO [171] Dactolisib Suppresses PI3K/Akt/mTOR signaling by inhibition of PI3K [226] Diallyl trisulfide Suppresses Wnt/β-catenin signaling [105] Epigallocatechin-3-gallate Suppresses Wnt signaling by upregulation of GSK-3β [96] Evodiamine Suppresses Wnt and Notch signaling [150] Farnesyl dimethyl chromanol Suppresses Wnt/β-catenin signaling [102] FH535 Suppresses Wnt/β-catenin signaling [123] GO-Y030 Suppresses JAK/STAT signaling by inhibition of STAT3 [195] GW6471 Suppresses PPAR signaling (PPARα antagonist) [204] Honokiol Suppresses Notch signaling by inhibition of the levels of the γ-secretase complex [139] HZ8CV2 Suppresses Wnt signaling [126] IC-2 Suppresses Wnt signaling [111] JIB-04 Suppresses Wnt signaling by increasing the expression of AXIN1 and GSK3β [109] LY294002 Suppresses PI3K/Akt/mTOR signaling by inhibition of PI3K [209] α-Mangostine Suppresses Notch signaling [155] Metformin Suppresses PI3K/Akt/mTOR signaling by inhibition of mTOR [231] Miransertib Suppresses PI3K/Akt/mTOR signaling by inhibition of Akt [210] MK-2206 Akt inhibitor [212] Napabucasin (BBI-608) Suppresses JAK/STAT signaling by inhibition of STAT3 [196] NCB-0846 Suppresses Wnt signaling by block TNIK [57,114] Phenet...…”

Section: -077mentioning

confidence: 99%

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Emerging agents that target signaling pathways to eradicate colorectal cancer stem cells

Silva

Santos

Dias

et al. 2021

Cancer Communications

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Colorectal cancer (CRC) represents the third most commonly diagnosed cancer and the second leading cause of cancer death worldwide. The modern concept of cancer biology indicates that cancer is formed of a small population of cells called cancer stem cells (CSCs), which present both pluripotency and self‐renewal properties. These cells are considered responsible for the progression of the disease, recurrence and tumor resistance. Interestingly, some cell signaling pathways participate in CRC survival, proliferation, and self‐renewal properties, and most of them are dysregulated in CSCs, including the Wingless (Wnt)/β‐catenin, Notch, Hedgehog, nuclear factor kappa B (NF‐κB), Janus kinase/signal transducer and activator of transcription (JAK/STAT), peroxisome proliferator‐activated receptor (PPAR), phosphatidyl‐inositol‐3‐kinase/Akt/mechanistic target of rapamycin (PI3K/Akt/mTOR), and transforming growth factor‐β (TGF‐β)/Smad pathways. In this review, we summarize the strategies for eradicating CRC stem cells by modulating these dysregulated pathways, which will contribute to the study of potential therapeutic schemes, combining conventional drugs with CSC‐targeting drugs, and allowing better cure rates in anti‐CRC therapy.

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Section: Cell Signaling Pathwaysmentioning

confidence: 99%

Section: -077mentioning

confidence: 99%

Emerging agents that target signaling pathways to eradicate colorectal cancer stem cells

Silva

Santos

Dias

et al. 2021

Cancer Communications

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show abstract

“…Therefore, many chemotherapeutics kill the malignant tumor bulk population, but CSCs can survive and cause recurrence [28,50]. Ning K et al reported that ATO decreased tumor growth, the conversion from colorectal CSCs to CRC cells, and augmented the density of CSCs [51]. The function of CSCs in lung cancer is maintained through signaling pathways such as WNT, Notch, and Hedgehog [28].…”

Section: Anti-cancer Mechanismsmentioning

confidence: 99%

Current Advances of Nanomedicines Delivering Arsenic Trioxide for Enhanced Tumor Therapy

Zhang

Fang

et al. 2022

Pharmaceutics

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Arsenic trioxide (ATO) is one of the first-line chemotherapeutic drugs for acute promyelocytic leukemia. Its anti-cancer activities against various human neoplastic diseases have been extensively studied. However, the clinical use of ATO for solid tumors is limited, and these limitations are because of severe systemic toxicity, low bioavailability, and quick renal elimination before it reaches the target site. Although without much success, several efforts have been made to boost ATO bioavailability toward solid tumors without raising its dose. It has been found that nanomedicines have various advantages for drug delivery, including increased bioavailability, effectiveness, dose-response, targeting capabilities, and safety as compared to traditional drugs. Therefore, nanotechnology to deliver ATO to solid tumors is the main topic of this review, which outlines the previous and present medical applications of ATO. We also summarised ATO anti-cancer mechanisms, limitations, and outcomes of combinatorial treatment with chemo agents. As a result, we strongly recommend conducting pre-clinical and clinical studies of ATO, especially nano-system-based ones that might lead to a novel combination therapy for cancer treatment with high efficacy, bioavailability, and low toxicity for cancer patients.

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“…Increased expression of ALDH1 is associated with tumor progression and poorer outcomes in CRC patients ( 11 ). ALDH1 is abundant in tumor samples from patients with CRC ( 21 , 84 ), which can be used as a particular marker for CSCs of colorectal cancer ( 85 ), mainly including ALDH1A1, ALDH1B1, and ALDH1A3, are associated with poor prognosis and resistance to chemotherapy in colorectal cancer ( 86 – 88 ).…”

Section: Aldh1 and Various Solid Tumorsmentioning

confidence: 99%

ALDH1: A potential therapeutic target for cancer stem cells in solid tumors

Wei

Chen

et al. 2022

Front. Oncol.

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Solid tumors can be divided into benign solid tumors and solid malignant tumors in the academic community, among which malignant solid tumors are called cancers. Cancer is the second leading cause of death in the world, and the global incidence of cancer is increasing yearly New cancer patients in China are always the first. After the concept of stem cells was introduced in the tumor community, the CSC markers represented by ALDH1 have been widely studied due to their strong CSC cell characteristics and potential to be the driving force of tumor metastasis. In the research results in the past five years, it has been found that ALDH1 is highly expressed in various solid cancers such as breast cancer, lung cancer, colorectal cancer, liver cancer, gastric cancer, cervical cancer, esophageal cancer, ovarian cancer, head,and neck cancer. ALDH1 can activate and transform various pathways (such as the USP28/MYC signaling pathway, ALDH1A1/HIF-1α/VEGF axis, wnt/β-catenin signaling pathway), as well as change the intracellular pH value to promote formation and maintenance, resulting in drug resistance in tumors. By targeting and inhibiting ALDH1 in tumor stem cells, it can enhance the sensitivity of drugs and inhibit the proliferation, differentiation, and metastasis of solid tumor stem cells to some extent. This review discusses the relationship and pathway of ALDH1 with various solid tumors. It proposes that ALDH1 may serve as a diagnosis and therapeutic target for CSC, providing new insights and new strategies for reliable tumor treatment.

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Effect of As2O3 on colorectal CSCs stained with ALDH1 in primary cell culture in�vitro

Cited by 3 publications

References 18 publications

Emerging agents that target signaling pathways to eradicate colorectal cancer stem cells

Emerging agents that target signaling pathways to eradicate colorectal cancer stem cells

Current Advances of Nanomedicines Delivering Arsenic Trioxide for Enhanced Tumor Therapy

ALDH1: A potential therapeutic target for cancer stem cells in solid tumors

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