Autophagy regulates cisplatin‐induced stemness and chemoresistance via the upregulation of <scp>CD</scp>44, <scp>ABCB</scp>1 and <scp>ADAM</scp>17 in oral squamous cell carcinoma

Naik, Prajna Paramita; Mukhopadhyay, Subhadip; Panda, Prashanta Kumar; Sinha, Niharika; Das, Chandan; Mishra, Rajakishore; Patil, Shankargouda; Bhutia, Sujit K.

doi:10.1111/cpr.12411

Cited by 87 publications

(54 citation statements)

References 41 publications

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“…Emerging evidences have illustrated the important roles of cancer stem‐like cells (CSC) in human tumours, including OSCC . In present study, our team aims to investigate the biological role of SNHG20 on the stemness and tumorigenesis of OSCC.…”

Section: Discussionmentioning

confidence: 99%

Long non‐coding RNA SNHG20 promotes the tumorigenesis of oral squamous cell carcinoma via targeting miR‐197/LIN28 axis

Zhao

Wang

et al. 2018

J Cellular Molecular Medi

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Long non‐coding RNA (lncRNA) has been verified to participate in the tumour regulation, including oral squamous cell carcinoma (OSCC). Nevertheless, the role of lncRNA SNHG20 on OSCC still remains elusive. Here, we investigate the physiopathologic functions of lncRNA SNHG20 in OSCC tumorigenesis and explore its potential mechanism. LncRNA SNHG20 was up‐regulated in OSCC tissue compared with adjacent non‐tumour tissue. Meanwhile, SNHG20 was overexpressed in cancer stem‐like cells. In vitro and in vivo, loss‐of‐function experiments showed that lncRNA SNHG20 knockdown inhibited proliferative ability, mammosphere‐forming ability, ALDH1 expression, stem factors (LIN28, Nanog, Oct4, SOX2) and tumour growth. Bioinformatics and luciferase reporter assay revealed that miR‐197 targeted the 3′‐untranslated regions of SNHG20 and LIN28 by complementary binding. Validation experiments confirmed the associated functions of SNHG20/miR‐197/LIN28 axis on OSCC proliferation and stemness. In summary, our results reveal the important function of SNHG20/miR‐197/LIN28 axis in the oncogenesis and stemness of OSCC, suggesting the vital role of SNHG20 in OSCC tumorigenesis.

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Section: Discussionmentioning

confidence: 99%

Long non‐coding RNA SNHG20 promotes the tumorigenesis of oral squamous cell carcinoma via targeting miR‐197/LIN28 axis

Zhao

Wang

et al. 2018

J Cellular Molecular Medi

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“…Yang et al reported that oxaliplatin-induced autophagy enriches the population of colorectal CD44 + CSCs and maintain the stemness of colorectal CSCs, this protection eventually causes chemoresistance in colorectal CSCs , and so did Nail's group. They found that autophagy regulates the expression of stemness surface marker CD44, drug resistance marker ABCB1 and invasion mediator ADAM17 to help maintain stemness and chemoresistance, but the mechanism remains unclear (Naik et al, 2018). Targeting autophagy to diminish the CSCs subpopulation might be a new direction to overcome platinum resistance.…”

Section: Autophagymentioning

confidence: 99%

The Drug-Resistance Mechanisms of Five Platinum-Based Antitumor Agents

et al. 2020

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Platinum-based anticancer drugs, including cisplatin, carboplatin, oxaliplatin, nedaplatin, and lobaplatin, are heavily applied in chemotherapy regimens. However, the intrinsic or acquired resistance severely limit the clinical application of platinum-based treatment. The underlying mechanisms are incredibly complicated. Multiple transporters participate in the active transport of platinum-based antitumor agents, and the altered expression level, localization, or activity may severely decrease the cellular platinum accumulation. Detoxification components, which are commonly increasing in resistant tumor cells, can efficiently bind to platinum agents and prevent the formation of platinum-DNA adducts, but the adducts production is the determinant step for the cytotoxicity of platinum-based antitumor agents. Even if adequate adducts have formed, tumor cells still manage to survive through increased DNA repair processes or elevated apoptosis threshold. In addition, autophagy has a profound influence on platinum resistance. This review summarizes the critical participators of platinum resistance mechanisms mentioned above and highlights the most potential therapeutic targets or predicted markers. With a deeper understanding of the underlying resistance mechanisms, new solutions would be produced to extend the clinical application of platinum-based antitumor agents largely.

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“…As described above, autophagy during treatment may reduce sensitivity to cytotoxic therapy. Correspondingly, resistance to various types of therapy is characterized by enhanced basal levels of autophagy, as defined by increased conversion of LC3‐I to LC3‐II, increased numbers of LC3B puncta per cell, upregulated numbers of autophagolysosomes, and degradation of p62 . For example, cisplatin‐resistant clones of ovarian cancer cell lines as well as an oral squamous cell carcinoma cell line were characterized by enhanced levels of autophagic flux .…”

Section: Part I: the Role Of Autophagy In Cancer Cellsmentioning

confidence: 99%

The multifaceted role of autophagy in cancer and the microenvironment

Folkerts

Hilgendorf

Vellenga

et al. 2018

Medicinal Research Reviews

164

143

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Autophagy is a crucial recycling process that is increasingly being recognized as an important factor in cancer initiation, cancer (stem) cell maintenance as well as the development of resistance to cancer therapy in both solid and hematological malignancies. Furthermore, it is being recognized that autophagy also plays a crucial and sometimes opposing role in the complex cancer microenvironment. For instance, autophagy in stromal cells such as fibroblasts contributes to tumorigenesis by generating and supplying nutrients to cancerous cells. Reversely, autophagy in immune cells appears to contribute to tumor‐localized immune responses and among others regulates antigen presentation to and by immune cells. Autophagy also directly regulates T and natural killer cell activity and is required for mounting T‐cell memory responses. Thus, within the tumor microenvironment autophagy has a multifaceted role that, depending on the context, may help drive tumorigenesis or may help to support anticancer immune responses. This multifaceted role should be taken into account when designing autophagy‐based cancer therapeutics. In this review, we provide an overview of the diverse facets of autophagy in cancer cells and nonmalignant cells in the cancer microenvironment. Second, we will attempt to integrate and provide a unified view of how these various aspects can be therapeutically exploited for cancer therapy.

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Autophagy regulates cisplatin‐induced stemness and chemoresistance via the upregulation of CD44, ABCB1 and ADAM17 in oral squamous cell carcinoma

Abstract: Objective: We inspected the relevance of CD44, ABCB1 and ADAM17 in OSCC stemness and deciphered the role of autophagy/mitophagy in regulating stemness and chemoresistance. Material and methods:

Cited by 87 publications

References 41 publications

Long non‐coding RNA SNHG20 promotes the tumorigenesis of oral squamous cell carcinoma via targeting miR‐197/LIN28 axis

Long non‐coding RNA SNHG20 promotes the tumorigenesis of oral squamous cell carcinoma via targeting miR‐197/LIN28 axis

The Drug-Resistance Mechanisms of Five Platinum-Based Antitumor Agents

The multifaceted role of autophagy in cancer and the microenvironment

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