The potential role of nicotine in breast cancer initiation, development, angiogenesis, invasion, metastasis, and resistance to therapy

Khodabandeh, Zhila; Valilo, Mohammad; Velaei, Kobra; Tazehkand, Abbas Pirpour

doi:10.1007/s12282-022-01369-7

Cited by 22 publications

(15 citation statements)

References 124 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…At present, there are data showing that nicotine can reduce the effect of chemotherapy on breast cancer and promote the generation of breast cancer stem cells [16]. Nicotine also plays an important role in the initiation, development, angiogenesis, invasion, metastasis and resistance to therapy of breast cancer [17]. The loss of tumor transcription regulation plays an important role in the biological function of the normal body, while taberrant regulation often leads to the occurrence and development of tumors, and nally it is the estrogen pathway.…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic and proteomic analysis of the mechanisms underlying the role of the CCT3 gene in breast cancer

Wang

et al. 2023

Preprint

View full text Add to dashboard Cite

Background Breast cancer has surpassed lung cancer as the most common cancer in the world. Our previous research showed that silencing the expression of the CCT3 gene significantly decreased the proliferation and metastasis of breast cancer cells, but the mechanism is still unclear. In this study, we investigated CCT3 gene and protein expression by transcriptomics and proteomics to explore the mechanism underlying its function. Methods MDA-MB-231 cells were transfected with CCT3-siRNA to knock down the expression of the CCT3 gene. qRT‒PCR was used to measure the efficiency of the suppression. We used RNA-seq and tandem mass tag proteomics analysis to identify differentially expressed genes and proteins, respectively. The possible biological consequences were determined by bioinformatics analysis. Results The mRNA expression of CCT3 decreased by 87.6% in MDA-MB-231 cells transfected with shCCT3 lentivirus. RNA-seq identified 449 differentially expressed genes after transfection with shCCT3, including 240 upregulated genes and 209 downregulated genes, and 61 differentially expressed proteins (33 upregulated and 28 downregulated) were identified by TMT proteomics analysis. GO and KEGG enrichment revealed the biological and molecular functions in CCT3-knockdown cells. Conjoint analysis revealed the expression of several genes and proteins, such as RPUSD4, LUC7L3, HELLS, ARL1, and SPINT2. Conclusions We explored the molecular mechanism by which the proliferation and metastasis of breast cancer cells are promoted after the expression of CCT3 is inhibited through transcriptomics and proteomics, and we initially identified several key genes and proteins. The functional verification of these genes requires further research.

show abstract

Section: Discussionmentioning

confidence: 99%

Transcriptomic and proteomic analysis of the mechanisms underlying the role of the CCT3 gene in breast cancer

Wang

et al. 2023

Preprint

View full text Add to dashboard Cite

show abstract

“…However, there is a lack in the evidence available about its potential genotoxic power; conversely, anti-inflammatory properties have been highlighted in vitro [ 57 ]. Nicotine is a characteristic alkaloid of the tobacco plant and its derived products [ 58 ], which has been reported to induce genotoxicity and genome instability in different preclinical studies [ 59 ]; however, it also suppresses DNA synthesis and the proliferation of leukemic cells [ 60 ]. Although the true mechanisms involved remain to be clarified, genetic injury by nicotine seems to be partly due to oxidative stress, which in turn could be regulated by a nicotinic receptor-dependent pathway [ 61 , 62 , 63 , 64 ].…”

Section: Discussionmentioning

confidence: 99%

β-Caryophyllene Counteracts Chemoresistance Induced by Cigarette Smoke in Triple-Negative Breast Cancer MDA-MB-468 Cells

et al. 2022

View full text Add to dashboard Cite

Exposure to cigarette smoke (CS) has been associated with an increased risk of fatal breast cancers and recurrence, along with chemoresistance and chemotherapy impairment. This strengthens the interest in chemopreventive agents to be exploited both in healthy and oncological subjects to prevent or repair CS damage. In the present study, we evaluated the chemopreventive properties of the natural sesquiterpene β-caryophyllene towards the damage induced by cigarette smoke condensate (CSC) in triple negative breast cancer MDA-MB-468 cells. Particularly, we assessed the ability of the sesquiterpene to interfere with the mechanisms exploited by CSC to promote cell survival and chemoresistance, including genomic instability, cell cycle progress, autophagy/apoptosis, cell migration and related pathways. β-Caryophyllene was found to be able to increase the CSC-induced death of MDA-MB-468 cells, likely triggering oxidative stress, cell cycle arrest and apoptosis; moreover, it hindered cell recovery, autophagy activation and cell migration; at last, a marked inhibition of the signal transducer and activator of transcription 3 (STAT3) activation was highlighted: this could represent a key mechanism of the chemoprevention by β-caryophyllene. Although further studies are required to confirm the in vivo efficacy of β-caryophyllene, the present results suggest a novel strategy to reduce the harmful effect of smoke in cancer patients and to improve the survival expectations in breast cancer women.

show abstract

“…Currently, breast cancer (BC) is considered one of the most common cancers, and according to global statistics in 2020, 2.26 million people were diagnosed with breast cancer, and this cancer is the main cause of death for women who die from cancer. Early diagnosis of the disease can prevent its progression and increase the survival rate ( 1 - 3 ). Based on histology, BC can be classified into two groups: invasive carcinoma and carcinoma in situ (CIS).…”

Section: Introductionmentioning

confidence: 99%

The nuclear factor erythroid 2-related factor 2/p53 axis in breast cancer

Fakheri,

Sajadi,

Afrashteh

et al. 2023

Biochem. med. (Online)

Self Cite

View full text Add to dashboard Cite

One of the most important factors involved in the response to oxidative stress (OS) is the nuclear factor erythroid 2-related factor 2 (Nrf2), which regulates the expression of components such as antioxidative stress proteins and enzymes. Under normal conditions, Kelch-like ECH-associated protein 1 (Keap1) keeps Nrf2 in the cytoplasm, thus preventing its translocation to the nucleus and inhibiting its role. It has been established that Nrf2 has a dual function; on the one hand, it promotes angiogenesis and cancer cell metastasis while causing resistance to drugs and chemotherapy. On the other hand, Nrf2 increases expression and proliferation of glutathione to protect cells against OS. p53 is a tumour suppressor that activates the apoptosis pathway in aging and cancer cells in addition to stimulating the glutaminolysis and antioxidant pathways. Cancer cells use the antioxidant ability of p53 against OS. Therefore, in the present study, we discussed function of Nrf2 and p53 in breast cancer (BC) cells to elucidate their role in protection or destruction of cancer cells as well as their drug resistance or antioxidant properties.

show abstract

The potential role of nicotine in breast cancer initiation, development, angiogenesis, invasion, metastasis, and resistance to therapy

Cited by 22 publications

References 124 publications

Transcriptomic and proteomic analysis of the mechanisms underlying the role of the CCT3 gene in breast cancer

Transcriptomic and proteomic analysis of the mechanisms underlying the role of the CCT3 gene in breast cancer

β-Caryophyllene Counteracts Chemoresistance Induced by Cigarette Smoke in Triple-Negative Breast Cancer MDA-MB-468 Cells

The nuclear factor erythroid 2-related factor 2/p53 axis in breast cancer

Contact Info

Product

Resources

About