Aldehyde Dehydrogenase 1 (ALDH1) Promotes the Toxicity of TRAIL in Non-Small Cell Lung Cancer Cells via Post-Transcriptional Regulation of MEK-1 Expression

Shen, Tian; Liu, Da-Hua; Wang, Dan; Ren, Fu; Pu, Xia

doi:10.1159/000495202

Cited by 7 publications

(2 citation statements)

References 27 publications

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“…Lung adenocarcinoma cells overexpressing ALDHA1A1 can meet rapid growth of tumor cells or respond to drug stress through the Warburg effect ( 58 ). High expression of ALDH1 can be achieved by activating the MEK/ERK signaling pathway ( 59 ). S100A9 upregulates ALDH1A1 expression and activates the RA signaling pathway in lung cancer cells ( 60 ).…”

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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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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“…Although CD44 was originally identified as a receptor for hyaluronic acid, it has also been suggested as a putative marker for various types of stem cells ( 48 , 49 ) and a key regulator for the maintenance of the properties of various CSCs ( 50 , 51 ). Aldehyde dehydrogenases (ALDH), a family of intracellular enzymes that catalyze cellular detoxification and subsequent drug resistance via oxidation of intracellular aldehydes, has been proposed as a putative biomarker for oral CSCs ( 52 ). Interestingly, ALDH-positive subpopulations isolated from head and neck squamous cell carcinoma have typical CSC characteristics and enhanced tumorigenic potential in vivo ( 53 , 54 ).…”

Section: Therapeutic Implications Of Oral Cscs In Cancer Therapymentioning

confidence: 99%

Targeting Cancer Stem Cell Markers or Pathways: A Potential Therapeutic Strategy for Oral Cancer Treatment

Lee

2021

IJSC

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Cancer stem cells (CSCs) are a small subset of cancer cells with stem cell-like properties, self-renewal potential, and differentiation capacity into multiple cell types. Critical genetic alterations or aberrantly activated signaling pathways associated with drug resistance and recurrence have been observed in multiple types of CSCs. In this context, CSCs are considered to be responsible for tumor initiation, growth, progression, therapeutic resistance, and metastasis. Therefore, to effectively eradicate CSCs, tremendous efforts have been devoted to identify specific target molecules that play a critical role in regulating their distinct functions and to develop novel therapeutics, such as proteins, monoclonal antibodies, selective small molecule inhibitors, and small antisense RNA (asRNA) drugs. Similar to other CSC types, oral CSCs can be characterized by certain pluripotency-associated markers, and oral CSCs can also survive and form 3D tumor spheres in suspension culture conditions. These oral CSC-targeting therapeutics selectively suppress specific surface markers or key signaling components and subsequently inhibit the stem-like properties of oral CSCs. A large number of new therapeutic candidates have been tested, and some products are currently in the pre-clinical or clinical development phase. In the present study, we review new oral CSC-targeted therapeutic strategies and discuss the various specific CSC surface markers and key signaling components involved in the stem-like properties, growth, drug resistance, and tumorigenicity of oral CSCs.

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