LRPPRC promotes glycolysis by stabilising LDHA mRNA and its knockdown plus glutamine inhibitor induces synthetic lethality via m A modification in triple-negative breast cancer.

Background: Targeted therapy for triple-negative breast cancer (TNBC) remains a challenge. N6-methyladenosine (m A) is the most abundant internal mRNA modification in eukaryotes, and it regulates the homeostasis and function of modified RNA transcripts in cancer. However, the role of leucine-rich pentatricopeptide repeat containing protein (LRPPRC) as an m A reader in TNBC remains poorly understood.

LncRNA CARMN suppresses EMT through inhibiting transcription of MMP2 activated by DHX9 in breast cancer.

Long non-coding RNAs (lncRNAs) have been shown to drive cancer progression. However, the function of lncRNAs and the underlying mechanism in early-stage breast cancer(BC) have rarely been investigated. Datasets of pre-invasive ductal carcinoma in situ (DCIS), invasive ductal BC (IDC) and normal breast tissue from TCGA and GEO databases were used to conduct bioinformatics analysis.

Transcriptionally regulated miR-26a-5p may act as BRCAness in Triple-Negative Breast Cancer.

Background: DNA damage and DNA damage repair (DDR) are important therapeutic targets for triple-negative breast cancer (TNBC), a subtype with limited chemotherapy efficiency and poor outcome. However, the role of microRNAs in the therapy is emerging. In this study, we explored whether miR-26a-5p could act as BRCAness and enhance chemotherapy sensitivity in TNBC.

mA reader HNRNPA2B1 destabilization of ATG4B regulates autophagic activity, proliferation and olaparib sensitivity in breast cancer.

N-methyladenosine RNA (mA) is the most extensive epigenetic modification in mRNA and influences tumor progression. However, the role of mA regulators and specific mechanisms in breast cancer still need further study. Here, we investigated the significance of the mA reader HNRNPA2B1 and explored its influence on autophagy and drug sensitivity in breast cancer.