lncRNA MALAT1 participates in metformin inhibiting the proliferation of breast cancer cell

Abstract

In recent years, the repurposing of conventional and chemotherapeutic drugs is recognized as an alternative strategy for health care. The main purpose of this study is to strengthen the application of non‐oncological drug metformin on breast cancer treatment in the perspective of epigenetics. In the present study, metformin was found to inhibit cell proliferation, promote apoptosis and induce cell cycle arrest in breast cancer cells at a dose‐dependent manner. In addition, metformin treatment elevated acH3K9 abundance and decreased acH3K18 level. The expression of lncRNA MALAT1, HOTAIR, DICER1‐AS1, LINC01121 and TUG1 was up‐regulated by metformin treatment. In metformin‐treated cells, MALAT1 knock‐down increased the Bax/Bcl2 ratio and enhanced p21 but decreased cyclin B1 expression. The expression of Beclin1, VDAC1, LC3‐II, CHOP and Bip was promoted in the cells received combinatorial treatment of metformin and MALAT1 knock‐down. The reduced phosphorylation of c‐Myc was further decreased in the metformin‐treated cells in combination with MALAT1 knock‐down than metformin treatment alone. Taken together, these results provide a promising repurposed strategy for metformin on cancer treatment by modulating epigenetic modifiers.

Ferroptosis and Cancer: Complex Relationship and Potential Application of Exosomes

“…These types of programmed cell death are all involved in cancer progression and therapy. In our lab, we focus on regulating the crosstalk among different types of programmed cell death to broaden the application of anti-tumor drugs ( Liu S. et al, 2017 ; Huang et al, 2018 , 2021a , b ; Xiang et al, 2019 ; Li T. et al, 2020 ). Inducing a certain type of programmed cell death specifically can have profound significance for cancer treatment.…”

Carnosic Acid Suppresses the Development of Oral Squamous Cell Carcinoma via Mitochondrial-Mediated Apoptosis

“…Apoptosis is a form of programmed cell death, mediated by multiple genes and cytokines, and constitutes an important target pathway to kill tumor cells (8,9). Cellular stress, DNA damage, and developmental signals all activate the endogenous apoptotic pathway (9)(10)(11).…”

“…Apoptosis is a form of programmed cell death, mediated by multiple genes and cytokines, and constitutes an important target pathway to kill tumor cells (8,9). Cellular stress, DNA damage, and developmental signals all activate the endogenous apoptotic pathway (9)(10)(11). Mitochondria are the primary source of intracellular reactive oxygen species (ROS) (12), which are oxygen-containing free radicals.…”

A New Nanomaterial Based on Extracellular Vesicles Containing Chrysin-Induced Cell Apoptosis Through Let-7a in Tongue Squamous Cell Carcinoma

“…(Yong et al, 2019).Moreover, EVs are endogenous and can carry noncoding RNAs (ncRNAs), mRNA, drugs, or peptides to have anticancer effects (Valadi et al, 2007;Kim et al, 2016). NcRNAs, such as miRNAs, have proven to have a role in cancer development (Di Leva et al, 2014;Huang et al, 2021). MiRNAs have 20-22 nucleotides and are abundant in EVs (Zhang et al, 2015).…”