Exosomal MALAT1 sponges miR-26a/26b to promote the invasion and metastasis of colorectal cancer via FUT4 enhanced fucosylation and PI3K/Akt pathway.

Background: Exosomes are vesicles of endocytic origin released by various cell types and emerging as important mediators in tumor cells. Human metastases-associated lung adenocarcinoma transcript 1 (MALAT1) is a long non-coding RNA known to promote cell proliferation, metastasis, and invasion in colorectal cancer (CRC).

Methods: The expression of MALAT1 was analyzed in CRC using qRT-PCR.

Retraction Note: Aberrant mannosylation profile and FTX/miR-342/ALG3-axis contribute to development of drug resistance in acute myeloid leukemia.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

The HOTAIR/miR-214/ST6GAL1 crosstalk modulates colorectal cancer procession through mediating sialylated c-Met via JAK2/STAT3 cascade.

Background: The regulatory non-coding RNAs, including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), emerge as pivotal markers during tumor progression. Abnormal sialylated glycoprotein often leads to the malignancy of colorectal cancer (CRC).

Methods: Differential levels of HOTAIR and ST6GAL1 are analyzed by qRT-PCR.

Correction to: LINC01296/miR-26a/GALNT3 axis contributes to colorectal cancer progression by regulating O-glycosylated MUC1 via PI3K/AKT pathway.

In the publication of this article [1], there is an error in Fig. 5C (panel 4, group of InmiR-26a + silinc01296 in SW620). The revised Fig.

Correction to: The regulatory ZFAS1/miR-150/ST6GAL1 crosstalk modulates sialylation of EGFR via PI3K/Akt pathway in T-cell acute lymphoblastic leukemia.

In the original publication of this article [1], there is a mistake in Fig. 4E.

MiR-29b/Sp1/FUT4 axis modulates the malignancy of leukemia stem cells by regulating fucosylation via Wnt/β-catenin pathway in acute myeloid leukemia.

Background: Acute myeloid leukemia (AML) is initiated and maintained by a unique, small subset of leukemia stem cells (LSCs). LSCs are characterized by unrestricted self-renewal and contribute to the malignancy of leukemia. Aberrant protein fucosylation is associated with AML progression.

The regulatory ZFAS1/miR-150/ST6GAL1 crosstalk modulates sialylation of EGFR via PI3K/Akt pathway in T-cell acute lymphoblastic leukemia.

Background: Noncoding RNAs, including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) are becoming key parts in the development of multidrug resistance (MDR) in T-cell acute lymphoblastic leukemia (T-ALL). Abnormal expression in sialyated N-glycans have been observed in MDR leukemia. However, the role of sialylation regulated MDR remains poorly understood.

Correction to: LINC01296/miR-26a/GALNT3 axis contributes to colorectal cancer progression by regulating O-glycosylated MUC1 via PI3K/AKT pathway.

In the publication of this article [1], there is an error in Fig. 5G (panel 2, group of InmiR-26a + siSCR in HCT-8/5-FU, treated with 284.3 μM).

HOTAIR/miR-326/FUT6 axis facilitates colorectal cancer progression through regulating fucosylation of CD44 via PI3K/AKT/mTOR pathway.

Metastasis is the main cause of death in colorectal cancer (CRC) patients. Aberrant fucosylation, catalyzed by the specific fucosyltransferases (FUTs), is associated with malignant behaviors. Non-conding RNAs, including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), emerge as key molecules in cancer malignancy.

LINC01296/miR-26a/GALNT3 axis contributes to colorectal cancer progression by regulating O-glycosylated MUC1 via PI3K/AKT pathway.

Background: Long non-coding RNAs (LncRNAs) emerging as pivotal marker in the procession of cancer, including colorectal cancer (CRC). Abnormal O-glycosylation is a crucial modification during cancer malignancy. The aim of this work is to analyze the alteration of O-glycosylation involved in CRC progression.

The potential of exosomes derived from colorectal cancer as a biomarker.

Colorectal cancer (CRC) is one of the most frequent causes of cancer death. The diagnosis and treatment for metastatic CRC and patients with drug resistance remains poor. Cancer cells characteristically produce and release exosomes, which act as a new signal pattern in the occurrence and development of tumors.

Aberrant mannosylation profile and FTX/miR-342/ALG3-axis contribute to development of drug resistance in acute myeloid leukemia.

Drug-resistance is a major problem in acute myeloid leukemia (AML) chemotherapy. Aberrant changes in specific N-glycans have been observed in leukemia multidrug resistance (MDR). MicroRNAs (miRNAs) and long non coding RNAs (lncRNAs) act as key players in the development of AML resistance to chemotherapy.