GEO series

CAMK1D activates PINK1/Parkin-dependent mitophagy to promote enzalutamide resistance in prostate cancer

GSE299843 Mus musculus (mouse) RNA-seq (gene expression) 2 samples Submitted 2025/06/30 Platform GPL19057

At a glance

RNA-seq (gene expression) · mouse · 2 samples

What it is: RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism: Mus musculus (mouse)
Samples: 2 samples
Data you can get: A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.

Summary (written by the submitters)

Although AR-targeted therapies (e.g., enzalutamide) initially improve outcomes of prostate cancer (PCa) patients, resistance inevitably develops, driven in part by prostate cancer stem-like cells (PCSCs). However, the molecular mechanisms linking PCSCs maintenance to enzalutamide resistance (ENZR) remain incompletely characterized. The emergence and reversal of ENZR represent critical clinical challenges in PCa therapeutics.

Read the full summary ↓

Cancer stem-like cells (CSCs) have been implicated in contributing to ENZR through multiple pathways. Here, we demonstrated that CAMK1D, a Ca²⁺/calmodulin-dependent kinase, is consistently upregulated in PCa with ENZR and contributes to resistance by enhancing mitophagy in PCa cells both in vitro and in vivo. Mechanistically, CAMK1D promotes the expansion of PCSCs by enhancing mitophagy through activation of the AMPK-PINK1 signaling pathway, thereby facilitating cellular adaptation. We reveal that CAMK1D interacts with AMPK, triggering lysosomal AMPK activation via metabolic stress–induced PINK1 phosphorylation. This AMPK-PINK1 cascade reprogramsmitochondrial metabolism to fuel PCSCs expansion. In patient-derived xenograft chimeras, targeting mitophagy or CAMK1D-AMPK signaling pathway suppresses tumor growth and depletes the PCSCs population. Our findings establish mitochondrial hemostasis as an important nexus between ENZR and AMPK-mediated PCSCs enrichment in PCa. CAMK1D emerges as a key regulator of ENZR by orchestrating mitophagy-dependent stemness maintenance. Therapeutically, we developed an Enz-siCAM/HNA nanoformulation that potently reverses ENZR and improves treatment responses.

This dataset

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Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE299843_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1277120 and SRA study SRP592416. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Samples in this study

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+ 2 more — browse all 2 samples with per-sample file links →

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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.