Long noncoding RNAs in the regulation of p53‐mediated apoptosis in human cancers

Chatterjee, Manjima; Viswanathan, Pragasam

doi:10.1002/cbin.11597

Cited by 8 publications

(7 citation statements)

References 140 publications

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“…The drug‐treated cells acquire activated damage repair mechanism, therefore, harbor functional p53 to promote cell‐cycle arrest (Upadhyay etl., 2016; Toma‐Jonik et al, 2019). Interestingly, the tumor suppressing or tumor driving lncRNAs regulate (regulators) or are regulated (effectors) by p53 to control transcriptional activity of genes involved in cell‐cycle arrest and apoptosis (Sanchez Calle et al, 2018, reviewed in Chatterjee & Viswanathan, 2021). It is tempting to demonstrate that in cancer cells SatIII colocalizes with p53 during the formation of nSBs.…”

Section: Discussionmentioning

confidence: 99%

Human satellite III long noncoding RNA imparts survival benefits to cancer cells

Chatterjee

Sengupta

2022

Cell Biology International

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Long noncoding RNAs (lncRNAs) are heterogeneous group of transcripts that lack coding potential and have essential roles in gene regulations. Recent days have seen an increasing association of noncoding RNAs with human diseases, especially cancers. One interesting group of noncoding RNAs strongly linked to cancers are heterochromatic repetitive Satellite RNAs. Satellite RNAs are transcribed from pericentromeric heterochromatic region of the human chromosomes. Satellite II RNA, most extensively studied, is upregulated in wide variety of epithelial cancer. Similarly, alpha satellite is over expressed in BRCA1‐deficient tumors. Though much is known about alpha satellites and SatII repeats, little is known about Satellite III (SatIII) lncRNAs in human cancers. SatIII repeats, though transcriptionally silent in normal conditions is actively transcribed under condition of stress, mainly heat shock. In this study, we show that colon and breast cancer cells aberrantly transcribes SatIII, in a heat shock factor I (HSF1)‐independent manner. Our study also reveals that, the overexpression of SatIII RNA favors cancer cell survival by overriding chemo drug‐induced cell death. Interestingly, knockdown of SatIII sensitizes cells toward chemotherapeutic drugs. This sensitization is possibly mediated by restoration of p53 protein expression that facilitates cell death. Heat shock however helps SatIII to continue with its pro‐cell survival function. Our results, therefore suggest SatIII to be an important regulator of human cancers. Induction of SatIII is not only a response to the oncogenic stress but also facilitates cancer progression by a distinct pathway that is different from heat stress pathway.

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Section: Discussionmentioning

confidence: 99%

Human satellite III long noncoding RNA imparts survival benefits to cancer cells

Chatterjee

Sengupta

2022

Cell Biology International

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“…p53 mutant has designated as a gain-ofoncogenic function(s) (GOFs) which improved cell migration, proliferation, as well as invasion with anti-apoptotic functions which dynamically contribute to numerous phases of tumor progression in cancer (Dittmer et al, 1993;Oren and Rotter, 2010). The changes beyond cancerous are subjected to deliberate discriminating benefits such as facilitating angiogenesis, continuous growth avoiding growth signal, insensitivity to cancer drugs, promotes adequate metabolism, escape from apoptosis with the self-sufficiency of stress signal and ultimately promoting metastasize and invasion (Chatterjee and Viswanathan, 2021;Hernandez Borrero and El-Deiry, 2021). Furthermore, growing evidences from in vitro and in vivo have signified that the oncogenic activities of p53 mutant variants have heterogeneous which can vary with tissue type in addition to genetic background of the cells (Eriksson et al, 2017).…”

Section: Role Of Mutant P53 Contributes To Autophagy Regulation In Cancermentioning

confidence: 99%

p53 Modulation of Autophagy Signaling in Cancer Therapies: Perspectives Mechanism and Therapeutic Targets

Rahman

Park

Rahman

et al. 2022

Front. Cell Dev. Biol.

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The key tumor suppressor protein p53, additionally known as p53, represents an attractive target for the development and management of anti-cancer therapies. p53 has been implicated as a tumor suppressor protein that has multiple aspects of biological function comprising energy metabolism, cell cycle arrest, apoptosis, growth and differentiation, senescence, oxidative stress, angiogenesis, and cancer biology. Autophagy, a cellular self-defense system, is an evolutionarily conserved catabolic process involved in various physiological processes that maintain cellular homeostasis. Numerous studies have found that p53 modulates autophagy, although the relationship between p53 and autophagy is relatively complex and not well understood. Recently, several experimental studies have been reported that p53 can act both an inhibitor and an activator of autophagy which depend on its cellular localization as well as its mode of action. Emerging evidences have been suggested that the dual role of p53 which suppresses and stimulates autophagy in various cencer cells. It has been found that p53 suppression and activation are important to modulate autophagy for tumor promotion and cancer treatment. On the other hand, activation of autophagy by p53 has been recommended as a protective function of p53. Therefore, elucidation of the new functions of p53 and autophagy could contribute to the development of novel therapeutic approaches in cancer biology. However, the underlying molecular mechanisms of p53 and autophagy shows reciprocal functional interaction that is a major importance for cancer treatment and manegement. Additionally, several synthetic drugs and phytochemicals have been targeted to modulate p53 signaling via regulation of autophagy pathway in cancer cells. This review emphasizes the current perspectives and the role of p53 as the main regulator of autophagy-mediated novel therapeutic approaches against cancer treatment and managements.

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“…Increasing evidence has shown that the mutational status and the functional regulation of TP53 in cancers are related to the disordered expression of lncRNAs directly or indirectly ( Aubrey et al, 2018 ). TP53, is considered the “guardian of the genome” and triggers cell apoptosis by inhibiting multiple pathways, and participates in the identification of DNA damage via DNA repair processes, thereby playing an important role in maintaining genomic stability ( Chatterjee and Viswanathan 2021 ). In other words, disrupting the “guardian of the genome” could force damaged cells into senescence or apoptosis, thereby accelerating the accumulation of somatic mutations.…”

Section: Discussionmentioning

confidence: 99%

Identification and Validation of HOTAIRM1 as a Novel Biomarker for Oral Squamous Cell Carcinoma

Niu

Zhang

et al. 2022

Front. Bioeng. Biotechnol.

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ORAL squamous cell carcinoma (OSCC) is a malignant tumor with the highest incidence among tumors involving the oral cavity maxillofacial region, and is notorious for its high recurrence and metastasis potential. Long non-coding RNAs (lncRNAs), which regulate the genesis and evolution of cancers, are potential prognostic biomarkers. This study identified HOTAIRM1 as a novel significantly upregulated lncRNA in OSCC, which is strongly associated with unfavorable prognosis of OSCC. Systematic bioinformatics analyses demonstrated that HOTAIRM1 was closely related to tumor stage, overall survival, genome instability, the tumor cell stemness, the tumor microenvironment, and immunocyte infiltration. Using biological function prediction methods, including Weighted gene co-expression network analysis (WGCNA), Gene set enrichment analysis (GSEA), and Gene set variation analysis (GSVA), HOTAIRM1 plays a pivotal role in OSCC cell proliferation, and is mainly involved in the regulation of the cell cycle. In vitro, cell loss-functional experiments confirmed that HOTAIRM1 knockdown significantly inhibited the proliferation of OSCC cells, and arrested the cell cycle in G1 phase. At the molecular level, PCNA and CyclinD1 were obviously reduced after HOTAIRM1 knockdown. The expression of p53 and p21 was upregulated while CDK4 and CDK6 expression was decreased by HOTAIRM1 knockdown. In vivo, knocking down HOTAIRM1 significantly inhibited tumor growth, including the tumor size, weight, volume, angiogenesis, and hardness, monitored by ultrasonic imaging and magnetic resonance imaging In summary, our study reports that HOTAIRM1 is closely associated with tumorigenesis of OSCC and promotes cell proliferation by regulating cell cycle. HOTAIRM1 could be a potential prognostic biomarker and a therapeutic target for OSCC.

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Long noncoding RNAs in the regulation of p53‐mediated apoptosis in human cancers

Cited by 8 publications

References 140 publications

Human satellite III long noncoding RNA imparts survival benefits to cancer cells

Human satellite III long noncoding RNA imparts survival benefits to cancer cells

p53 Modulation of Autophagy Signaling in Cancer Therapies: Perspectives Mechanism and Therapeutic Targets

Identification and Validation of HOTAIRM1 as a Novel Biomarker for Oral Squamous Cell Carcinoma

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